ArticleCancer medicine2017
miR-1 suppresses the proliferation and promotes the apoptosis of esophageal carcinoma cells by targeting Src.
Article in Cancer medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- UpZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Construction of long non-coding RNA- and microRNA-mediated competing endogenous RNA networks in alcohol-related esophageal cancer.PloS one · 2022Article
- Synthetic Evaluation of MicroRNA-1-3p Expression in Head and Neck Squamous Cell Carcinoma Based on Microarray Chips and MicroRNA Sequencing.BioMed research international · 2021Article
- Suppression of long non-coding RNA MALAT1 inhibits survival and metastasis of esophagus cancer cells by sponging miR-1-3p/CORO1C/TPM3 axis.Molecular and cellular biochemistry · 2020Article
- Identification and validation of hub microRNAs dysregulated in esophageal squamous cell carcinoma.Aging · 2020Article
- Long noncoding antisense RNA FAM83A-AS1 promotes lung cancer cell progression by increasing FAM83A.Journal of cellular biochemistry · 2019Article
- MALAT1 silencing suppresses prostate cancer progression by upregulating miR-1 and downregulating KRAS.OncoTargets and therapy · 2018Article
- miR-1 suppresses the proliferation and promotes the apoptosis of esophageal carcinoma cells by targeting Src.Cancer medicine · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonreceptor tyrosine kinase c-Src, also known as Src, is a potent oncogene involved in a series of biological processes including cell growth, differentiation, and apoptosis; however, its expression pattern and function in esophageal cancer is poorly addressed. In this study, abnormal overexpression of Src protein was observed in esophageal cancer tissues, which fuelled the speculation that microRNA-mediated posttranscriptional regulatory mechanism might be involved. Bioinformatic analyses were applied to identify miRNAs that could potentially target Src. miR-1 was predicted and further validated as a direct repressor of Src. Moreover, we manipulated knockdown and overexpression experiment on TE-1 and TE-10 cells to demonstrate miR-1 suppressed proliferation and promoted apoptosis in esophageal cancer cells by inhibiting Src. Taken together, this study underlines a negative regulatory mechanism in which miR-1 serves as a suppressor of Src in esophageal cancer cells and may provide insights into novel therapeutic approaches for esophageal cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.