Tagged: colorectal cancer

Precision Oncology in Metastatic Colorectal Cancer: A Real-World Case Study

September 24, 2025

“Heavily pretreated metastatic colorectal cancer (mCRC) poses significant therapeutic challenges.”

Colorectal cancer is one of the most common—and deadliest—cancers worldwide. Once it spreads and reaches the metastatic stage, treatment becomes far more difficult. Tumors can also behave very differently from one patient to another, especially after multiple rounds of therapy. Precision oncology is helping to overcome these challenges by enabling clinicians to analyze each tumor’s unique genetic profile and tailor treatment accordingly.

This approach was recently highlighted in a case study published in Volume 16 of Oncotarget. The report detailed how a 62-year-old man with advanced colorectal cancer received a highly personalized treatment plan, developed by an international panel of experts, after completing all standard treatment options.

The Case: Personalized Cancer Care in Action

Titled “Case Report WIN-MTB-2023001: WIN International Molecular Tumor Board – A 62-year-old male with metastatic colorectal cancer with 5 prior lines of treatment,” the paper illustrates how precision medicine can be applied in real-world cancer care. The paper was led by Alberto Hernando-Calvo from Vall d’Hebron University Hospital and Vall d’Hebron Institute of Oncology; Razelle Kurzrock from WIN Consortium and Medical College of Wisconsin; Oncotarget Editor-in-Chief Wafik S. El-Deiry from WIN Consortium and Legorreta Cancer Center at Brown University; and corresponding author Shai Magidi, also from WIN Consortium.

The patient had already undergone five different treatment regimens, including chemotherapy and targeted therapies. While some approaches initially showed results, the cancer repeatedly returned. With standard options exhausted, his case was submitted to the WIN International Molecular Tumor Board (MTB)—a global network of cancer experts representing 13 countries.

Comprehensive tumor genetic profiling revealed mutations in key genes such as BRAF, MET, APC, TP53, and NRAS. These alterations are known to promote tumor growth, contribute to treatment resistance, and predict a poor prognosis. Based on these findings, the MTB proposed a series of personalized treatment strategies, using off-label drug combinations designed to target the tumor’s specific genetic vulnerabilities.

Results: A Multi-Drug Treatment Approach

The team proposed several personalized treatment options. One strategy combined amivantamab (a dual-action antibody against MET and EGFR), trametinib (a MEK inhibitor), and regorafenib (a multi-target drug with effects on VEGF and WNT pathways). These combinations were not standard but were based on previous responses and the patient’s mutational profile. The plan was to start with reduced doses to avoid side effects, a method supported by earlier studies. Though access to some drugs was uncertain outside the United States, the goal was to attack the tumor from multiple angles based on its unique weaknesses.

The Breakthrough: Rethinking Cancer Therapy with Precision Oncology

This case highlights a key innovation in cancer treatment—not a new drug, but a new way of thinking. Instead of relying on a one-size-fits-all approach, clinicians matched the therapy to the patient’s tumor genetic characteristics. Importantly, these decisions were developed collaboratively and in real time by an international panel of experts.

The Impact: Expanding Options for Patients with Advanced Tumors

If applied more broadly, this personalized strategy could improve outcomes for patients with hard-to-treat cancers. Especially for those who have failed standard treatments, precision oncology can offer a way forward when no other effective options remain. It is a shift from treating cancer generally to treating the individual behind the diagnosis.

Future Perspectives and Conclusion

Although the patient in this case ultimately passed away, his case shows how much progress has been made in precision medicine. With detailed genetic testing and input from experts around the world, it is now possible to create treatment plans that would have been unthinkable just a few years ago. This case highlights the urgent need for wider access to advanced testing and new treatments, especially in countries where some drugs may not be available. Precision medicine is no longer just an idea for the future; it has become a present-day necessity in complex cancer care.

Click here to read the full Precision Oncology in Oncotarget.

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Oncotarget is an open-access, peer-reviewed journal that has published primarily oncology-focused research papers since 2010. These papers are available to readers (at no cost and free of subscription barriers) in a continuous publishing format at Oncotarget.com.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Panitumumab and Low-Dose Capecitabine: A Promising Maintenance Therapy for Metastatic Colorectal Cancer

May 7, 2025

“Considerations around maintenance therapy are of particular importance when drugs associated with cumulative neurotoxicity like Oxaliplatin form part of adopted regimens.”

A recent study from Assiut University Hospital in Egypt, published in Oncotarget, presents a promising strategy for patients with metastatic colorectal cancer (mCRC). The research introduces a gentler yet effective maintenance therapy that may extend survival, enhance quality of life, and offer a more accessible treatment option for mCRC patients worldwide.

The Challenge of Treating Metastatic Colorectal Cancer

Colorectal cancer is one of the most common causes of cancer-related deaths worldwide. When it spreads to other parts of the body—a stage known as mCRC—it becomes much more difficult to treat. At this stage, clinicians often use strong drug combinations like FOLFOX or CAPOX, which mix chemotherapy drugs to stop cancer growth. FOLFOX combines three drugs given intravenously, while CAPOX includes two of the same drugs, with one taken as a pill.

While effective, these treatments can cause serious side effects. For example, one of the main drugs, oxaliplatin, can lead to nerve damage, making it painful or difficult to use the hands and feet. Fatigue, diarrhea, and other issues are also common. Over time, these side effects may force clinicians to stop or adjust the treatment, even if it is working.

That is where maintenance therapy comes in. After the cancer is controlled, clinicians often switch to a gentler treatment plan to keep it from returning. The challenge is finding a therapy that continues to work without causing too many side effects, especially in places where access to expensive or intensive treatments is limited.

The Study: A Targeted, Low-Intensity Maintenance Option for Metastatic Colorectal Cancer

In the study titled “Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen,” recently published in Volume 16 of Oncotarget, researchers Doaa A. Gamal, Aiat Morsy, and Mervat Omar from Assiut University Hospital focused on a combination of two well-established drugs. Panitumumab is a targeted therapy that blocks a protein called EGFR, which helps cancer cells grow and divide. Capecitabine is a chemotherapy drug that turns into 5-fluorouracil inside the body to stop cancer cell growth.

Instead of delivering Capecitabine in high, occasional doses, the researchers used a low, continuous dose—a method known as metronomic dosing—designed to reduce side effects while maintaining anti-cancer effects.

The study involved 25 patients with mCRC who had a specific genetic profile: wild-type KRAS and BRAF, meaning they did not have mutations in those genes. All patients first received six rounds of standard chemotherapy plus Panitumumab. Those who responded well were then switched to the maintenance phase: Panitumumab every two weeks, along with daily low-dose Capecitabine.

The Results: Longer Survival and Better Tolerability

Patients in this study experienced an average of 18 months without their cancer getting worse—a period known as progression-free survival (PFS). By comparison, patients without maintenance therapy typically see a PFS of only 4–8 months. Their overall survival—the average time they lived after starting treatment—reached 45 months, far exceeding the 12 to 30 months reported in earlier studies with more intensive regimens.

Patients whose cancer had spread at the same time as their initial diagnosis (called synchronous metastasis) had even better outcomes, with PFS extending beyond 23 months.

The treatment was also well-tolerated. Only 8% of patients experienced severe side effects such as skin rash or diarrhea, and those symptoms were managed with standard care. No one had to stop or change their treatment due to side effects.

The Breakthrough: A Simpler Approach to Metastatic Colorectal Cancer Maintenance

This study is one of the first to explore Panitumumab in combination with metronomic Capecitabine as a maintenance strategy. The results suggest that using this combination in a low-intensity, long-term setting can keep the disease stable while minimizing the harsh effects of more aggressive therapies. Because both drugs are already approved and widely used, this regimen could be more easily implemented—especially for mCRC patients who have responded well to earlier treatments.

Importantly, this strategy may also help delay resistance to Panitumumab, which is a common issue when targeted therapies are used over time.

The Impact: Expanding Access to Safer Long-Term Colorectal Cancer Care

For many mCRC patients—particularly those in countries with limited healthcare—access to affordable and tolerable treatments is a major barrier. By using widely available medications in a simpler format, this regimen could help make effective maintenance therapy more accessible to a broader group of patients. Compared with other maintenance regimens studied in large trials, this approach showed similar or better results with fewer serious side effects.

Future Perspectives and Conclusion

Though this was a small study conducted at a single center, the findings are promising. Panitumumab combined with low-dose Capecitabine could be a safe and effective maintenance option for patients with wild-type KRAS and BRAF mCRC, especially those who start with strong responses and limited side effects.

Larger trials will be needed to confirm these results. However, if future research supports this strategy, it could transform the management of mCRC from high-intensity, short-term treatments to sustainable, patient-friendly care that supports long-term well-being.

Click here to read the full research paper in Oncotarget.

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Oncotarget

How a Simple Blood Test Could Predict Colorectal Cancer Surgery Success

February 26, 2025

“The concentration of cell-free DNA (cfDNA) before and after surgery may be related to the prognosis of patients with CRC, but there is limited information regarding cfDNA levels at the time of surgery.”

Imagine if a single blood test could tell clinicians in real time how successful a cancer surgery has been. A recent study from the University of Brasília, published in Oncotarget, suggests that such an approach might soon be possible. By tracking changes in cell-free DNA (cfDNA) levels before, during, and after colorectal cancer (CRC) surgery, researchers have found a potential new way to monitor tumor removal and predict patient outcomes.

Cell-Free DNA and Colorectal Cancer Surgery

Cell-free DNA consists of tiny fragments of genetic material that are released into the bloodstream when cells break down. In healthy individuals, these fragments come from normal cell turnover, but in cancer patients, some of this DNA originates from tumor cells. cfDNA detection has been used to track cancer progression and treatment response in diseases like lung, breast, and CRC. What had not been investigated until now was how cfDNA levels fluctuate during cancer surgery itself.

Since surgery is the primary treatment for CRC, understanding how cfDNA levels change during surgical intervention could provide valuable insights into whether the tumor has been fully removed and how the patient’s body reacts to the procedure.

The Study: Measuring Cell-Free DNA in Real-Time

In the study, titled “Assessment of cfDNA release dynamics during colorectal cancer surgery,” led by first author Mailson Alves Lopes and corresponding author Fabio Pittella-Silva, scientists analyzed blood plasma samples from 30 CRC patients at three critical time points—before, during, and after surgery. Using highly sensitive genetic tests, they measured changes in cfDNA concentration to determine whether surgery had a direct impact on its release. The goal was to check whether cfDNA could serve as a biomarker for evaluating surgical effectiveness and predicting the probability of cancer recurrence.

The Challenge: Improving Colorectal Cancer Surgery Outcomes

Despite advances in CRC treatment, up to 50% of patients experience cancer recurrence after surgery. One of the greatest challenges in cancer care is determining whether surgery has successfully removed all cancer cells. Current methods rely on imaging scans and periodic biomarker testing, which can take months to detect any signs of recurrence.

A real-time way to assess surgical success, such as monitoring cfDNA levels, could transform how clinicians track cancer patients, allowing for more informed decisions about follow-up treatments and postoperative care.

The Results: A Significant Spike in Cell-Free DNA Levels

The researchers found that cfDNA levels increased nearly three times during surgery and remained elevated after the procedure. This increase was even more pronounced in specific groups of patients. People over 60, people who already had diabetes or heart disease, and people who had high levels of carcinoembryonic antigen (CEA), a known cancer marker, had the highest cfDNA spikes.

Patients with larger or more aggressive tumors showed even greater cfDNA release during surgery, likely due to increased tissue damage. Furthermore, surgeries that lasted longer were also linked to higher levels of cfDNA, suggesting that more cells are breaking down, leading to more genetic material entering the bloodstream.

The Breakthrough: A Potential Game-Changer in Colorectal Cancer Monitoring

This study is the first to show that cfDNA levels can reflect the extent of surgical intervention in real time. Monitoring cfDNA during surgery could help determine whether a tumor has been fully removed and whether additional treatment is needed. For instance, if cfDNA levels remain high after surgery, it could indicate the presence of cancer cells undetectable by regular imaging. Such findings could lead to earlier treatment and closer monitoring.

The Impact in Colorectal Cancer Treatment

If validated in further studies, cfDNA testing could become a standard tool in CRC surgery. Real-time tracking of cfDNA levels could help personalize postoperative care by identifying high-risk patients, guiding follow-up treatments, and detecting potential recurrence sooner. Additionally, cfDNA may serve as a quality marker for surgical procedures, ensuring better patient outcomes.

The Future Perspectives and Conclusion

While these findings are promising, further research is needed to standardize cfDNA testing for surgical monitoring. Larger clinical trials will be essential to confirm its ability to predict cancer recurrence and surgical success. With continued advancements, a simple blood test could soon help clinicians optimize cancer surgeries and improve patient outcomes, from the operating room to long-term recovery.

Click here to read the full research paper in Oncotarget.

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Oncotarget

Combining Regorafenib and TAS102 to Target Gastrointestinal Cancers and Overcome Cancer Stemness

August 9, 2024

In this research paper, researchers demonstrate a promising new treatment option for refractory metastatic gastrointestinal cancers using a combination of two FDA-approved drugs.

Researchers Jun Zhang, Lanlan Zhou, Shuai Zhao, and Wafik S. El-Deiry from Fox Chase Cancer Center and Brown University explore the potential of combining TAS102 (trifluridine/tipiracil) and regorafenib as a treatment option for gastrointestinal (GI) cancers. Their research paper, published in Oncotarget’s Volume 15 on July 2, 2024, is entitled, “Regorafenib synergizes with TAS102 against multiple gastrointestinal cancers and overcomes cancer stemness, trifluridine-induced angiogenesis, ERK1/2 and STAT3 signaling regardless of KRAS or BRAF mutational status.”

The Study

The combination of two FDA-approved drugs, TAS102 and regorafenib, has shown promising results in preclinical studies. TAS102 is an oral formulation consisting of trifluridine (FTD) and tipiracil hydrochloride (TPI). It has been approved by the US FDA for the treatment of refractory metastatic colorectal cancer and metastatic gastric cancer. Regorafenib is a multi-target tyrosine kinase inhibitor that inhibits tumor angiogenesis and cell proliferation and is approved for the treatment of gastrointestinal cancers.

Recent studies have shown that TAS102, in combination with regorafenib, can lead to improved survival and restrict tumor progression. The combination therapy has been found effective in multiple gastrointestinal cancer cell lines, including colorectal, gastric, and pancreatic cancers.

Cancer stem cells (CSCs) are a subpopulation of cancer cells that contribute to tumor growth, recurrence, and chemo-resistance. Targeting CSCs can be an effective approach to overcoming therapy resistance and preventing tumor progression. TAS102, in combination with regorafenib, has been shown to reduce the stemness of colorectal cancer cells, inhibiting the formation of colonospheres and reducing the CD133+ subpopulation.

Tumor angiogenesis, the formation of new blood vessels, is essential for tumor growth and metastasis. TAS102 monotherapy has been found to promote angiogenesis in tumors harboring a BRAF mutation. However, when combined with regorafenib, TAS102-induced angiogenesis is abrogated, as regorafenib inhibits the formation of microvessels in xenografted tumors.

The combination therapy of TAS102 and regorafenib regulates several signaling pathways, including ERK1/2 and STAT3, and modulates the expression of thymidylate synthase (TS), which is involved in drug resistance.

Conclusion

The combination of TAS102 and regorafenib shows synergistic effects in preclinical studies, inhibiting tumor growth, reducing the stemness of cancer cells, and inhibiting angiogenesis. Further research is needed to explore the efficacy of this combination therapy in clinical settings and to identify potential biomarkers of drug sensitivity. The TAS102 plus regorafenib drug combination may be further tested in gastric and other GI cancers.

“Recent studies have shown that TAS102 in combination with regorafenib can lead to improved survival and restrict tumor progression.”

Click here to read the full research paper in Oncotarget.

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Oncotarget is an open-access, peer-reviewed journal that publishes primarily oncology-focused research papers. These papers are available to readers (at no cost and free of subscription barriers) in a continuous publishing format at Oncotarget.com.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative), and Dimensions (Digital Science).

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Oncotarget

Triple Combination Treatment Overcomes Colorectal Cancer Resistance

December 14, 2023

In a new study, researchers aimed to elucidate the role of cancer stemness in the resistance of colorectal cancer cells to targeted therapies.

Triple Combination Treatment Overcomes Colorectal Cancer Resistance

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Colorectal cancer is the third most diagnosed cancer and the second leading cause of cancer-related deaths worldwide. It often starts in the colon or rectum with small, noncancerous clumps of cells called polyps, which can develop into cancer over time. Risk factors for colorectal cancer include age, family history, inflammatory bowel diseases, diet, smoking, and physical activity.

The development and progression of colorectal cancer are driven by the aberrant activation of multiple signaling pathways, such as EGFR (epidermal growth factor receptor), RAS-RAF, and PTEN-PI3K. Among these pathways, the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathways are particularly important, as they are frequently mutated in colorectal cancer. Therapeutic targeting of these pathways has shown promise in suppressing tumor growth. However, cancer cells often develop resistance to targeted therapies, leading to treatment failure and disease progression.

In a new study, researchers Astha Lamichhane, Gary D. Luker, Seema Agarwal, and Hossein Tavana from The University of Akron, University of Michigan and Georgetown University aimed to elucidate the role of cancer stemness in the resistance of colorectal cancer cells to targeted therapies. Their research paper was published in Oncotarget on October 4, 2023, entitled, “Inhibiting BRAF/EGFR/MEK suppresses cancer stemness and drug resistance of primary colorectal cancer cells.”

The Study

One of the major mechanisms of drug resistance in cancer is the gain of stemness in cancer cells under drug pressure. Cancer stem cells (CSCs) are a small subpopulation of cells within a tumor with the ability to self-renew and differentiate into various cell types that constitute the tumor. CSCs are thought to be responsible for tumor initiation, progression, and resistance to therapy. Therefore, identifying approaches to target CSCs is crucial for improving treatment outcomes in colorectal cancer patients.

In the current study, the researchers developed spheroid cultures of patient-derived BRAFmut and KRASmut tumor cells and studied the resistance mechanisms to inhibition of the MAPK pathway. The researchers found that treatment with MAPK pathway inhibitors enriched the expression of CSC markers CD166, ALDH1A3, CD133, and LGR5 and activated the PI3K/Akt pathway in cancer cells. These findings suggest that the development of drug resistance in colorectal cancer is associated with the acquisition of a stem cell-like phenotype.

To overcome drug resistance mediated by cancer stemness, the researchers examined various combination treatments to block these activities. They found that a triple combination treatment targeting BRAF, EGFR, and MEK significantly reduced stemness and the activities of oncogenic signaling pathways in colorectal cancer cells. This triple combination treatment has shown promise in clinical trials, with response rates of 21% and 32% in patients with BRAFmut colorectal cancer. The researchers demonstrated that this combination treatment effectively suppressed the growth, stemness, and activities of several oncogenic signaling pathways in cancer cells.

“Our finding supports the hypothesis that CSCs confer drug resistance and suppressing stemness is a viable approach in BRAFmut colorectal cancer.”

Conclusion

Altogether, the researchers found that inhibiting BRAF, EGFR, and MEK in combination shows promise in suppressing cancer stemness and overcoming drug resistance in colorectal cancer cells. This approach targets the underlying mechanisms of resistance, providing a potential strategy for improving treatment outcomes in patients with colorectal cancer. Further research and clinical trials are needed to validate the efficacy and safety of this triple combination therapy.

“In conclusion, this study presented a model of cyclic drug treatment and recovery of patient-derived tumor spheroids and established that single-agent MEK inhibition of colorectal cancer cells lead to adaptive resistance of cancer cells through gain of stemness. A triple combination treatment used in a clinical trial of colorectal cancer patients effectively blocked growth, stemness, and activities of several oncogenic signaling pathways in cancer cells. Our approach to identify mechanisms of drug resistance of patient-derived cancer cells to targeted therapies and develop effective treatments is promising toward cancer precision medicine.”

Click here to read the full research paper in Oncotarget.

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Can the Creatine Shuttle be Targeted to Fight Colorectal Cancer?

May 25, 2023

In a new study, researchers investigated the creatine shuttle pathway as a potential therapeutic target in colorectal cancer cells.

Can the Creatine Shuttle be Targeted to Fight Colorectal Cancer?

Listen to an audio version of this article

Since the 1992 Barcelona Olympics, creatine supplementation has increased in popularity and grown to widespread use among the mainstream public. Creatine is a naturally occurring compound, primarily stored in skeletal muscle and involved in energy production for high-intensity activities—enhancing performance and supporting muscle growth and strength. The process by which creatine is transported into the muscles and utilized for energy production is referred to as the creatine shuttle. While it is a useful mechanism for healthy muscles, the creatine shuttle has also been implicated in cancer.

“The creatine shuttle is highlighted in cancer as a source of energy for cancer cells that display aggressive proliferation, and aberrant creatine kinase (CK) levels are known to be associated with many malignancies and mitotic control [7].”

In a new study, researchers Mayu Kita, Rina Fujiwara-Tani, Shingo Kishi, Shiori Mori, Hitoshi Ohmori, Chie Nakashima, Kei Goto, Takamitsu Sasaki, Kiyomu Fujii, Isao Kawahara, Ujjal Kumar Bhawal, Yi Luo, and Hiroki Kuniyasu from Nara Medical University, Saveetha University and Nantong University hypothesized that the creatine shuttle is involved in energy metabolism and other adenosine triphosphate (ATP) supply in cancer cells. On May 19, 2023, their new research paper was published in Oncotarget’s Volume 14, entitled, “Role of creatine shuttle in colorectal cancer cells.”

“In the current study, the role of the creatine shuttle in CRC [colorectal cancer] was analyzed along with its potential as a therapeutic target.”

The Creatine Shuttle in Colorectal Cancer

Despite advancements in treatment options for colorectal cancer (CRC), incidence and mortality rates remain high. The metabolism of CRC cells is distinctly different from that of normal cells, and understanding these metabolic alterations is crucial for devising new targeted therapies. The creatine shuttle system plays a pivotal role in cellular energy metabolism, particularly in high-energy demanding tissues such as muscle and brain. However, its involvement in CRC cells has remained largely unexplored until now.

Creatine kinase, also known as CK or creatine phosphokinase, is an enzyme that catalyzes the transfer of a phosphate group from creatine phosphate to adenosine diphosphate (ADP), thereby regenerating adenosine triphosphate (ATP), which is the primary energy source for cells. CK exists in different forms or isoenzymes. In this study, the researchers investigated the expression and role of creatine kinase B (CKB) and mitochondrial creatine kinase (MTCK) in CRC tissues. They also explored the inhibitory effect of dinitrofluorobenzene (DNFB) on CKB and MTCK activity and its impact on CRC cell growth, stemness, mitochondrial function, energy metabolism, and cancer metastasis.

Inhibition of the Creatine Shuttle

The team used tissue arrays to examine CKB and MTCK expression in CRC tissues. Both proteins were highly expressed in high-grade tumors and cases with distant metastasis. Liver metastases showed higher expression compared to primary tumors, suggesting a role in CRC progression and metastasis.

DNFB, an inhibitor of CK activity, reduced CK activity and inhibited cell growth in CT26 and HT29 CRC cell lines. HT29 cells, with higher CKB and MTCK levels, were less sensitive to DNFB than CT26 cells. DNFB treatment decreased cell number, stem cell marker expression and impaired sphere formation in CT26 and HT29 cells. Knockdown of CKB or MTCK showed similar effects, indicating specificity to CK inhibition. DNFB also inhibited mitochondrial function and energy metabolism, decreasing mitochondrial membrane potential, increasing ROS production, and reducing OCR and ATP production in both cell lines.

In a mouse model of peritoneal dissemination, pretreatment with DNFB reduced tumor growth. Excised tumors from DNFB-treated mice showed decreased proliferation and stem cell marker expression, as well as reduced phosphorylation levels of tumor-promoting signaling molecules (EGFR, AKT, and ERK1/2).

Summary & Conclusion

“In this study, we showed that inhibition of the creatine shuttle by blocking CKB and MTCK activity suppressed the growth, stemness, and metastasis of cancer. It was suggested that the cause of this is related to inhibition of both mitochondrial energy metabolism and the phosphorylation signaling system.”

This research study provides valuable insights into the role of CKB and MTCK in CRC and highlights the therapeutic potential of inhibiting the creatine shuttle in CRC treatment. Inhibition of CKB and MTCK activity by DNFB impaired CRC cell growth, stemness, mitochondrial function, energy metabolism, and cancer metastasis. These findings suggest that targeting the creatine shuttle pathway may represent a promising therapeutic strategy for CRC patients. Further studies are warranted to validate these findings and explore the potential of targeting the creatine shuttle in clinical settings.

“Our data suggest that the antitumor effect of creatine shuttle inhibition can be attributed to the inhibition of mitochondrial energy production as well as the inhibition of multiple phosphorylation signals through inhibition of the ATP supply. Therefore, it is necessary to develop a new CK inhibitor to induce these two effects in vivo.”

Click here to read the full research paper in Oncotarget.

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