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MiR-96 promotes proliferation and chemo- or radioresistance by down-regulating RECK in esophageal cancer
- Source :
- Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 68(8)
- Publication Year :
- 2014
-
Abstract
- The involvement of miR-96 in esophageal cancer (EC) remains unclear. The aim of this study is to explore the functional role of miR-96 and determine whether miR-96 could be a potential therapeutic target for human esophageal cancer. MiR-96 up-regulation was demonstrated in 145 EC samples and RECK down-regulation was validated in EC cell lines. Moreover, ectopic overexpression of miR-96 in TE-1 or ECa-109 contributed to tumor growth in xenograft mouse models. Furthermore, up-regulation of miR-96 could reduce the susceptibilities of EC cells to chemotherapy or radiotherapy. RECK was identified as a target of miR-96 and RECK overexpressing could abrogate the growth of EC cells induced by miR-96. Taken together, miR-96 serves as an oncogene role in EC cells through downregulating RECK.
- Subjects :
- Functional role
Male
Pathology
medicine.medical_specialty
Esophageal Neoplasms
medicine.medical_treatment
Down-Regulation
Mice, Nude
Antineoplastic Agents
Biology
GPI-Linked Proteins
Mice
Radioresistance
Cell Line, Tumor
medicine
Animals
Humans
Tumor growth
Aged
Pharmacology
Chemotherapy
Mice, Inbred BALB C
Oncogene
General Medicine
Esophageal cancer
Middle Aged
medicine.disease
Radiation therapy
MicroRNAs
Cell culture
Drug Resistance, Neoplasm
Cancer research
Female
Subjects
Details
- ISSN :
- 19506007
- Volume :
- 68
- Issue :
- 8
- Database :
- OpenAIRE
- Journal :
- Biomedicinepharmacotherapy = Biomedecinepharmacotherapie
- Accession number :
- edsair.doi.dedup.....46f71bec0eafaf3a364971c17dd58dca