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MiR-135a promotes gastric cancer progression and resistance to oxaliplatin.


ABSTRACT: Resistance to oxaliplatin (OXA)-based chemotherapy regimens continues to be a major cause of gastric cancer (GC) recurrence and metastasis. We analyzed GC samples and matched non-tumorous control stomach tissues from 280 patients and found that miR-135a was overexpressed in GC samples relative to control tissues. Tumors with high miR-135a expression were more likely to have aggressive characteristics (high levels of carcino-embryonic antigen, vascular invasion, lymphatic metastasis, and poor differentiation) than those with low levels. Patients with greater tumoral expression of miR-135a had shorter overall survival times and times to disease recurrence. Furthermore, miR-135a, which promotes the proliferation and invasion of OXA-resistant GC cells, inhibited E2F transcription factor 1 (E2F1)-induced apoptosis by downregulating E2F1 and Death-associated protein kinase 2 (DAPK2) expression. Our results indicate that higher levels of miR-135a in GC are associated with shorter survival times and reduced times to disease recurrence. The mechanism whereby miR-135a promotes GC pathogenesis appears to be the suppression of E2F1 expression and Sp1/DAPK2 pathway signaling.

SUBMITTER: Yan LH 

PROVIDER: S-EPMC5342584 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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miR-135a promotes gastric cancer progression and resistance to oxaliplatin.

Yan Lin-Hai LH   Chen Zhi-Ning ZN   Li-Li   Chen Jia J   Wei Wen-E WE   Mo Xian-Wei XW   Qin Yu-Zhou YZ   Lin Yuan Y   Chen Jian-Si JS  

Oncotarget 20161001 43


Resistance to oxaliplatin (OXA)-based chemotherapy regimens continues to be a major cause of gastric cancer (GC) recurrence and metastasis. We analyzed GC samples and matched non-tumorous control stomach tissues from 280 patients and found that miR-135a was overexpressed in GC samples relative to control tissues. Tumors with high miR-135a expression were more likely to have aggressive characteristics (high levels of carcino-embryonic antigen, vascular invasion, lymphatic metastasis, and poor dif  ...[more]

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