Management of colorectal cancer

Brown, Kilian G. M.; Solomon, Michael J.; Mahon, Kate; O’Shannassy, Sarah

doi:10.1136/bmj.l4561

Cited by 65 publications

(55 citation statements)

References 47 publications

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“…Its morbidity and mortality can be mitigated through proper screening and surveillance [2]. Treatments for colorectal cancer include endoscopic and surgical procedures, chemotherapy and radiotherapy [3]. Colonic stenting is also a palliative therapy for unresectable colon cancer [4].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Chen

et al. 2020

Cancer Cell Int

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Background Colorectal cancer ranks among the most lethal diseases worldwide. Although much progress has been made in research and treatment of colorectal cancer in recent years, the underlying mechanisms related to migration of the cancer cells and the reason for chemoresistance still remain unclear. In this research, we explored the underlying effect of miR-138-5p in colorectal cancer. Methods We used qRT-PCR to investigate the expression of miR-138-5p, Snail1, NFIB in colorectal cancer cells. Lentiviral vectors containing miR-138-5p mimics and inhibitors were constructed and transfected cells. Wound healing assay was applied to illustrate interferences on cell migration. Fluorouracial, doxorubicin, cisplat in were used to detect chemotherapy resistance. In order to identify target genes, bioinformatic methods were applied. Snail1 and NFIB protein expression in stable cell lines was detected using Western blot. Double luciferase and CHIP experiment were used to verify binding sites. We used rescue experiments to further explore the interactions among Snail1, NFIB and miR-138-5p. Results The expression of miR-138-5p in colorectal cancer cells was low. miR-138-5p inhibited cell migration in colorectal cancer, and could negatively regulate chemotherapy resistance. miR-138-5p targeted NFIB, and regulated Snail1 expression, which mediated colorectal cancer cell migration and chemotherapy resistance. Conclusions Our research indicates that miR-138-5p could be a crucial modulator controlling colorectal cancer cell migration and chemoresistance, by acting upon the NFIB-Snail1 axis. miR-138-5p has an emerging prospect to be exploited as a new target for colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Chen

et al. 2020

Cancer Cell Int

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“…Of note, in some cases, chemotherapy or radiotherapy might be applied before or after surgery as neoadjuvant or adjuvant treatment to maximally reduce and stabilize the tumor. [9][10][11][12] Chemotherapy Current chemotherapy includes both single-agent therapy, which is mainly fluoropyrimidine (5-FU)-based, and multipleagent regimens containing one or several drugs, including oxaliplatin (OX), irinotecan (IRI), and capecitabine (CAP or XELODA or XEL). Although studies have argued that first-line single-agent therapy is not inferior to combined regimens in terms of overall survival (OS), 13,14 the combined therapy regimens FOLFOX (5-FU+OX), FOXFIRI (5-FU+IRI), XELOX or CAPOX (CAP+OX), and CAPIRI (CAP+OX) remain the mainstream approaches in first-line treatment, while patients with poor performance or at low risk of deterioration are recommended to receive single-agent therapy.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive review of targeted therapy for colorectal cancer

Xie

Chen

Fang

2020

Sig Transduct Target Ther

1,135

821

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Colorectal cancer (CRC) is among the most lethal and prevalent malignancies in the world and was responsible for nearly 881,000 cancer-related deaths in 2018. Surgery and chemotherapy have long been the first choices for cancer patients. However, the prognosis of CRC has never been satisfying, especially for patients with metastatic lesions. Targeted therapy is a new optional approach that has successfully prolonged overall survival for CRC patients. Following successes with the anti-EGFR (epidermal growth factor receptor) agent cetuximab and the anti-angiogenesis agent bevacizumab, new agents blocking different critical pathways as well as immune checkpoints are emerging at an unprecedented rate. Guidelines worldwide are currently updating the recommended targeted drugs on the basis of the increasing number of high-quality clinical trials. This review provides an overview of existing CRC-targeted agents and their underlying mechanisms, as well as a discussion of their limitations and future trends.

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“…Although great advances have been recently achieved in the management of colorectal cancer, the long-term outcomes of this common malignancy remain unsatisfactory, 3 which is mainly because of the tumor occurrence and chemotherapy resistance. 31,32 The success of MSC-based therapy for colorectal cancer has been documented in both experimental and clinical models; however, there are still a number of questions that remain to be investigated.…”

Section: Discussionmentioning

confidence: 99%

“…2 Currently, the management of colorectal cancer mainly depends on surgery, chemotherapy and radiotherapy. 3 Despite great advances in the therapy of colorectal cancer, the outcomes of patients with advanced colorectal cancer remain poor and the 5-year survival rate is unsatisfactory due to tumor recurrence and metastasis and drug resistance. 4,6 A search for novel treatments to improve the prognosis of patients with colorectal cancer is therefore given a high priority.…”

Section: Introductionmentioning

confidence: 99%

<p>Rat Bone Marrow-Derived Mesenchymal Stem Cells Promote the Migration and Invasion of Colorectal Cancer Stem Cells</p>

Zou¹,

Zhao²,

Li³

et al. 2020

OTT

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Background: Colorectal cancer is one of the most common cancers and the second leading cause of cancer-related deaths worldwide. Targeting cancer stem cells (CSCs) may be a novel strategy for the treatment of colorectal cancer. Previous studies have shown that bone marrowderived MSCs (BM-MSCs) promote tumor growth and metastasis. However, the role of rat BM-MSCs in the biological behaviors of colorectal CSCs remains unclear until now. Materials and Methods: BM-MSCs were isolated from rats and characterized. CSCs were enriched from HCT116 cells using the microsphere culture method, and the microspheres incubated for at least 10 passages were termed HCT116-CSCs that were characterized. The effects of rat BM-MSCs on migration and invasion of HCT116-CSCs were examined using transwell migration and invasion assays and xenograft tumor growth assay. Results: Rat BM-MSCs appeared typical stem cell morphology. Flow cytometry revealed positive CD29 and CD44 expression in rat BM-MSCs at passage 3, and rat BM-MSCs were found to differentiate into osteocytes following incubation in osteogenic induction medium. Microscopy, flow cytometric detection of stem cell surface markers, colony-formation assay and transwell migration and invasion assays characterized the successful preparation of HCT116-CSCs, and subcutaneous injection of HCT116-CSCs produced xenograft tumors in nude mice, while HE staining of the xenograft tumors displayed cancer specimen shapes. Transwell migration and invasion assays showed that rat BM-MSCs promoted the migration and invasion of HCT116-CSCs, and injection of rat BM-MSCs was found to promote the growth of the mouse xenograft tumor derived from HCT116-CSCs. Conclusion: Rat BM-MSCs promote the migration and invasion of colorectal CSCs, and colorectal CSCs may be a potential target for the therapy against colorectal cancer.

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Management of colorectal cancer

Cited by 65 publications

References 47 publications

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Comprehensive review of targeted therapy for colorectal cancer

<p>Rat Bone Marrow-Derived Mesenchymal Stem Cells Promote the Migration and Invasion of Colorectal Cancer Stem Cells</p>

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