ArticleCancer medicine2018
MiR-634 sensitizes glioma cells to temozolomide by targeting CYR61 through Raf-ERK signaling pathway.
Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Role of Non-coding RNAs in the Response of Glioblastoma to Temozolomide.Molecular neurobiology · 2025Review
- Loss of miR-634 contributes to the formation FOXA1-positive triple negative breast cancer subtype.Discover oncology · 2024Article
- Article
- Decoding microRNA drivers in atherosclerosis.Bioscience reports · 2022Review
- MicroRNA-25 promotes cell proliferation, migration and invasion in glioma by directly targeting cell adhesion molecule 2.Experimental and therapeutic medicine · 2022Article
- MSC-AS1 knockdown inhibits cell growth and temozolomide resistance by regulating miR-373-3p/CPEB4 axis in glioma through PI3K/Akt pathway.Molecular and cellular biochemistry · 2021Article
- LncRNA SNHG8 Serves as an Oncogene in Breast Cancer Through miR-634/ZBTB20 Axis.Cancer management and research · 2021Article
- LINC00210 exerts oncogenic roles in glioma by sponging miR-328.Experimental and therapeutic medicine · 2020Article
- MiR-3116 sensitizes glioma cells to temozolomide by targeting FGFR1 and regulating the FGFR1/PI3K/AKT pathway.Journal of cellular and molecular medicine · 2020Article
- Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis.Cancer management and research · 2020Article
- MicroRNA-634 functions as a tumor suppressor in pancreatic cancer via directly targeting heat shock-related 70-kDa protein 2.Experimental and therapeutic medicine · 2019Article
- microRNA-605 directly targets SOX9 to alleviate the aggressive phenotypes of glioblastoma multiforme cell lines by deactivating the PI3K/Akt pathway.OncoTargets and therapy · 2019Article
- Enhanced Inhibition of Tumorigenesis Using Combinations of miRNA-Targeted Therapeutics.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is the most common intracranial malignant tumors, accounting for about 40% of intracranial tumors. Primary or secondary drug resistance is one of the main reasons for the failure of treatment. The oncogenic or tumor-suppressive roles of miR-634 have been revealed in different types of cancer. However, the role of miR-634 in glioma remains unknown and whether miR-634 could sensitize glioma cells to temozolomide also is unclear. Here, we aim to investigate the biological function of miR-634 and the possible mechanisms in glioma. In this study, we found that miR-634 was downregulated in glioma tissues compared with normal brain tissues, and its expression was associated with tumor size and WHO grade. Importantly, glioma patients with low miR-634 expression showed a shorter survival time than patients which had high expression of miR-634. This study also showed that miR-634 was decreased in temozolomide-resistant glioma cells, and restoration of miR-634 could sensitize the resistant cells to temozolomide by targeting CYR61 through Raf-ERK signaling. Our study provides a potential target for overcome drug resistance in glioma.
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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.