Differential effects of the LncRNA RNF157-AS1 on epithelial ovarian cancer cells through suppression of DIRAS3- and

Pengfei Xu1, Sujuan Xu2,3, Haiyue Pan2,4

  • 1Nanjing Maternity and Child Health Care Institute, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), 210004, Nanjing, China. pengfeixu@njmu.edu.cn.

Cell Death & Disease
|February 22, 2023
PubMed

Insights

The long non-coding RNA RNF157-AS1 promotes epithelial ovarian cancer (EOC) progression and chemoresistance by inhibiting autophagy. Suppressing RNF157-AS1 may offer a therapeutic strategy for EOC patients undergoing chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Epithelial ovarian cancer (EOC) is a leading cause of cancer-related deaths in women.
  • Long non-coding RNAs (lncRNAs) play critical roles in cancer development and progression.
  • RNF157 Antisense RNA 1 (RNF157-AS1) is implicated in various cancers, but its role in EOC remains unclear.

Purpose of the Study:

  • To investigate the role of RNF157-AS1 in EOC proliferation, invasion, and migration.
  • To elucidate the molecular mechanisms underlying RNF157-AS1's function in EOC.
  • To evaluate the potential of RNF157-AS1 as a therapeutic target in EOC chemotherapy.

Main Methods:

  • Database analysis and cell culture experiments to assess RNF157-AS1 expression and function.
  • RNA pulldown, RIP, mass spectrometry, and ChIP assays to identify RNF157-AS1 interacting proteins and binding sites.
  • Western blot, immunofluorescence, and CCK8 assays to analyze protein expression, autophagy levels, and chemosensitivity.

Main Results:

  • RNF157-AS1 is overexpressed in EOC tissues and promotes EOC cell proliferation, invasion, and migration.
  • RNF157-AS1 interacts with HMGA1 and EZH2 to suppress ULK1 and DIRAS3 expression, respectively, thereby inhibiting autophagy.
  • RNF157-AS1 overexpression enhances EOC cell sensitivity to cisplatin (DDP) chemotherapy by suppressing autophagy, leading to longer overall survival (OS) and progression-free survival (PPS).

Conclusions:

  • RNF157-AS1 acts as an oncogenic lncRNA in EOC by inhibiting autophagy.
  • RNF157-AS1-mediated suppression of autophagy enhances EOC cell sensitivity to DDP chemotherapy.
  • RNF157-AS1 represents a promising therapeutic target for improving chemotherapy outcomes in EOC patients.

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