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Long-Chain Non-Coding RNA SNHG3 Promotes the Growth of Ovarian Cancer Cells by Targeting miR-339-5p/TRPC3 Axis.
Liu, En-Ling; Zhou, Yu-Xiu; Li, Jun; Zhang, Dong-Hong; Liang, Feng.
Afiliación
  • Liu EL; The Department of Obstetrics and Gynecology, Tangshan Gongren Hospital Affiliated to Hebei Medical University, Tangshan, Hebei Province, People's Republic of China.
  • Zhou YX; The Department of Immunology, Tangshan Gongren Hospital Affiliated to Hebei Medical University, Tangshan, Hebei Province, People's Republic of China.
  • Li J; The Department of Obstetrics and Gynecology, Tangshan Gongren Hospital Affiliated to Hebei Medical University, Tangshan, Hebei Province, People's Republic of China.
  • Zhang DH; The Department of Obstetrics and Gynecology, Tangshan Gongren Hospital Affiliated to Hebei Medical University, Tangshan, Hebei Province, People's Republic of China.
  • Liang F; The Department of Obstetrics and Gynecology, Tangshan Gongren Hospital Affiliated to Hebei Medical University, Tangshan, Hebei Province, People's Republic of China.
Onco Targets Ther ; 13: 10959-10971, 2020.
Article en En | MEDLINE | ID: mdl-33149611
ABSTRACT

BACKGROUND:

Long-chain non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is reportedly overexpressed in malignant tumors, but its regulatory role in human ovarian cancer (OC) is not fully understood.

METHODS:

A qRT-PCR assay was carried out to detect the level of SNHG3 in OC tissues, serum and cells, a CCK-8 assay to measure the proliferation of OC cells, a transwell assay to measure the invasion and migration of OC cells, and a flow cytometry to detect the cell cycle distribution and apoptosis rate of OC cells. In addition, in vivo experiment was also conducted to determine the effect of SNHG3 on the growth of OC cells.

RESULTS:

SNHG3 was overexpressed in OC tissues, serum, and cells, and the overexpression in serum indicated a poor prognosis of patients. It was also found that knockdown of SNHG3 could inhibit the malignant phenotypes of OC cells, cause G1/G0 cell cycle arrest, and intensify apoptosis. Furthermore, in in vitro experiments, the growth ability of OC cells was inhibited under knockdown of SNHG3. Assays for relationship verification showed that SNHG3 regulated the expression of miR-339-5p and the canonical transient receptor potential 3 (TRPC3), and the rescue experiment revealed that co-transfection of si-SNHG3+miR-339-5p-inhibitor or si-SNHG3+pcDNA3.1-TRPC3 could reverse the effects of knockdown of SNHG3 on the biological behavior of OC cells.

CONCLUSION:

SNHG3 can be adopted as a marker for diagnosis and prognosis evaluation of OC and it plays a role in the progression of OC by enabling the miR-339-5p sponge to regulate TRPC3 expression.
Palabras clave

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Onco Targets Ther Año: 2020 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Onco Targets Ther Año: 2020 Tipo del documento: Article