c‐Met inhibition enhances chemosensitivity of human ovarian cancer cells

Wang, Jing; Cheng, Jianxin

doi:10.1111/1440-1681.12672

Cited by 16 publications

(20 citation statements)

References 21 publications

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“…Capmatinib (INC280) blocks c-Met phosphorylation and the activation of key downstream molecules in c-Met-dependent tumor cell lines, causing mitochondrial membrane depolarization and DNA repair [ 96 , 97 ]. The drug has been utilized in phase I trials for advanced solid cancer.…”

Section: Current Clinical Trials Targeting C-metmentioning

confidence: 99%

“…The drug has been utilized in phase I trials for advanced solid cancer. Wei et al [ 96 ] found that the addition of capmatinib could effectively block cell proliferation induced by cancer associated fibroblast (CAF) matrix with overexpression of HGF, and could eliminate CAF-induced ovarian cancer cell resistance. The latest study by Lara et al [ 97 ] utilized a series of NSCLC cell lines (including three EGFR-mutant cell lines, HCC827, PC9 and H1975, one Kirsten rat sarcoma virus oncogene mutant cell line, H358, and one EGFR and KRAS wild type cell line, H1666) to determine whether capmatinib in combination with erlotinib could attenuate erlotinib resistance.…”

Section: Current Clinical Trials Targeting C-metmentioning

confidence: 99%

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Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities

et al. 2018

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c-Met is a receptor tyrosine kinase belonging to the MET (MNNG HOS transforming gene) family, and is expressed on the surfaces of various cells. Hepatocyte growth factor (HGF) is the ligand for this receptor. The binding of HGF to c-Met initiates a series of intracellular signals that mediate embryogenesis and wound healing in normal cells. However, in cancer cells, aberrant HGF/c-Met axis activation, which is closely related to c-Met gene mutations, overexpression, and amplification, promotes tumor development and progression by stimulating the PI3K/AKT, Ras/MAPK, JAK/STAT, SRC, Wnt/β-catenin, and other signaling pathways. Thus, c-Met and its associated signaling pathways are clinically important therapeutic targets. In this review, we elaborate on the molecular structure of c-Met and HGF and the mechanism through which their interaction activates the PI3K/AKT, Ras/MAPK, and Wnt signaling pathways. We also summarize the connection between c-Met and RON and EGFR, which are also receptor tyrosine kinases. Finally, we introduce the current therapeutic drugs that target c-Met in primary tumors, and their use in clinical research.

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Section: Current Clinical Trials Targeting C-metmentioning

confidence: 99%

Section: Current Clinical Trials Targeting C-metmentioning

confidence: 99%

Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities

et al. 2018

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“…The tyrosine kinase c-Met, also called MET and hepatocyte growth factor receptor (HGFR), is a key regulator of organ development and cancer progression and has been studied in many cancer types such as lung cancer, gastric cancer, prostate cancer and so on [ 4 – 7 ]. c-Met inhibitors also have been tested in many cancers and shown promising results in lung cancer, ovarian cancer and so on [ 5 , 8 ]. In breast cancer, previous studies have yielded mixed results.…”

Section: Introductionmentioning

confidence: 99%

Clinicopathological and prognostic significance of c-Met overexpression in breast cancer

Zhao

Hui

et al. 2017

Oncotarget

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Backgroundc-Met has been shown to promote organ development and cancer progression in many cancers. However, clinicopathological and prognostic value of c-Met in breast cancer remains elusive.MethodsPubMed and EMBASE databases were searched for eligible studies. Correlation of c-Met overexpression with survival data and clinicopathological features was analyzed by using hazard ratio (HR) or odds ratio (OR) and fixed-effect or random-effect model according to heterogeneity. All statistical tests were two-sided.Results32 studies with 8281 patients were analyzed in total. The c-Met overexpression was related to poor OS (overall survival) (HR=1.65 (1.328, 2.051)) of 18 studies with 4751 patients and poor RFS/DFS (relapse/disease free survival) (HR=1.53 (1.20, 1.95)) of 12 studies with 3598 patients. Subgroup analysis according to data source/methods/ethnicity showed c-Met overexpression was related to worse OS and RFS/DFS in Given by author group, all methods group and non-Asian group respectively. Besides, c-Met overexpression was associated with large tumor size, high histologic grade and metastasis.ConclusionsOur results showed that c-Met overexpression was connected with poor survival rates and malignant activities of cancer, including proliferation, migration and invasion, which highlighted the potential of c-Met as significant candidate biomarker to identify patients with breast cancer at high risk of tumor death.

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“…Blocking c-Met expression may overcome the resistance of cancer cells to cisplatin [34]. After treatment with crizotinib, cisplatin-induced proliferation inhibition and apoptosis were observed [35]. The long-term efficacy of crizotinib was found in several malignant tumors with MET amplification such as gastric and renal carcinoma [36,37].…”

Section: Gene Mutation In Omctsmentioning

confidence: 99%

Recurrence of ovarian squamous cell carcinoma with MET gene copy number variation: a case report and review of literature

2020

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Background: Malignant transformation such as ovarian squamous cell carcinoma (SCC) in ovarian mature cystic teratoma (OMCT) is a rare tumor. The gene mutation of ovarian SCC remains unclear. We herein report a recurrent case of ovarian squamous cell carcinoma with MET gene copy number variation. Case presentation: A 60-year-old woman presented with recurrence of ovarian SCC 8 months after primary surgery. Adhesiolysis, right abdominal wall mass excision, prosthetics, enterectomy, enterostomy and partial cystectomy were performed by laparoscope. Pathologic examination demonstrated metastatic squamous cell carcinoma in ileocecus, rectum and abdominal wall muscle. MET gene copy number was elevated with copy number of six in this case. Postoperatively, the patient was treated with four cycles of combination chemotherapy with docetaxel and carboplatin. The patient was free of disease at 20 months' follow-up. Conclusions: Optimal cytoreductive surgery combined with platinum-based chemotherapy is recommended currently for not only primary tumor but also recurrence. For patients with malignant transformation in OMCT, prompt diagnosis and individualized treatment are crucial for better prognosis. Increased copy number of MET may be correlated with her poor PFS and can be a potential therapeutic target for this case.

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c‐Met inhibition enhances chemosensitivity of human ovarian cancer cells

Cited by 16 publications

References 21 publications

Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities

Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities

Clinicopathological and prognostic significance of c-Met overexpression in breast cancer

Recurrence of ovarian squamous cell carcinoma with MET gene copy number variation: a case report and review of literature

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