Related Experiment Video

Updated: Aug 24, 2026

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

MicroRNA320e Augments the Synthetic Lethality of Olaparib by Regulating the PI3K-AKT-mTOR Pathway

Wei Zheng1, Qianlong Meng1,2, Yunhan Deng1

  • 1Department of Gynecology, Fuxing Hospital, Capital Medical University, Beijing, China.

Oncology Research
|August 22, 2026
PubMed
Abstract

Insights

MicroRNA320e (miR-320e) overexpression inhibits ovarian cancer progression and enhances sensitivity to olaparib. This finding offers a new strategy to overcome drug resistance in ovarian cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer (OC) exhibits increasing drug resistance, particularly to poly ADP-ribose polymerase inhibitors (PARPi) used for homologous recombination repair defects (HRD).
  • MicroRNA320e (miR-320e) is recognized for its negative regulatory role in various cancer progressions.

Purpose of the Study:

  • To investigate the association between miR-320e and drug resistance in ovarian cancer.
  • To determine the therapeutic potential of miR-320e in overcoming PARPi resistance.

Main Methods:

  • Cell Counting Kit-8 (CCK-8), migration, invasion, and colony formation assays were used to assess cellular functions.
  • Western blot (WB) analysis examined signaling pathway protein expression.
  • In vivo studies utilized a xenograft subcutaneous tumor model.
  • Immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) detected protein and miR-320e expression.

Main Results:

  • miR-320e overexpression reduced proliferation, invasion, and migration while enhancing autophagy and apoptosis in ovarian cancer cells.
  • The PI3K-AKT-mTOR signaling pathway was significantly inhibited by miR-320e.
  • Overexpression of miR-320e suppressed tumor growth in mouse models and increased sensitivity to olaparib.

Conclusions:

  • miR-320e overexpression inhibits ovarian cancer malignancy.
  • Increased miR-320e levels enhance the sensitivity of ovarian cancer cells to olaparib therapy, suggesting a potential therapeutic strategy.
Keywords:
MicroRNA320e (miR-320e)PI3K-AKT-mTORfibronectin 1 (FN1)olaparibpoly ADP-ribose polymerase inhibitors (PARPi)

More Related Videos

Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer09:40

Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...