ETV5 overexpression

Overexpression of MALAT1 in Sertoli cells did not induce apoptosis but impaired their cell supporting function. In conclusion, MALAT1 overexpression in SSCs contributes to the pathogenesis of iNOA via downregulating ETV5 expression and promoting cell apoptosis.

In addition, TGFβ1 and TGFβ3 were downregulated in the absence of ETV5. ETV5 silencing induces epithelial phenotype by downregulating TGFβ1 and TGFβ3 in INS-1 (832/13) cell line.

Elevated ETV5 expression promotes NSCLC cell invasion and migration via transcriptional activates of TGFβ1. Therefore, ETV5/TGFβ signaling may serve as a therapeutic target for NSCLS patients.

ETV5 promoted metastasis of ESCC by activating MMPs through augmenting the transcription of SKA1 and TRPV2. ETV5 was likely to be a novel oncogene and therapeutic target in ESCC.

ETV5 has a carcinogenic effect in HGSOC and can be used as a clinically effective biomarker to determine the prognosis of HGSOC patients.

LncRNA HCG18 acted as a sponge of miR-148b and played an oncogenic role in osteosarcoma, providing therapeutic targets for osteosarcoma.

Moreover, ETV5 changed drug-sensitivity to palbociclib and dinaciclib. Therefore, therapeutic regimens targeting ETV5 may be promising in improving the efficacy of target-CDK treatment in CRC.