Target intelligence / Profile preview

MicroRNA 520g (miR-520g)

Target
miR-520g
Molecular classification
microRNA, Non-coding RNA, Gene regulator
01

Overview

MicroRNA 520g (miR-520g) is a short non-coding RNA that post-transcriptionally regulates gene expression by binding to the 3′ untranslated regions of mRNA targets, primarily acting as a gene silencer. It is part of the miR-520 family and is implicated in oncogenic processes, including promotion of cell proliferation, invasion, and resistance to chemotherapy in several human cancers. Notably, miR-520g mediates drug resistance in colorectal and ovarian cancer by downregulating key tumor suppressors (p21/CDKN1A in colon cancer[1], DAPK2 in ovarian cancer[2]), thereby facilitating cell cycle progression and reduced apoptosis. It is upregulated in various cancers, particularly in cases associated with chemoresistance and poor prognosis. Expression levels of miR-520g may serve as both a prognostic and predictive biomarker for response to chemotherapy. In stem cell-like and primitive cancer populations, miR-520g is associated with maintenance of undifferentiated states and can regulate expression of pro-thrombotic proteins such as tissue factor (TF)[3]. As an emerging target, therapeutic modulation of miR-520g is under investigation for its potential to sensitize tumors to standard chemotherapies and inhibit cancer progression.

Other names
hsa-mir-520gMIRN520Gmir-520gMIR520G
02

Mechanism of action

Drug resistance via post-transcriptional suppression of tumor suppressors (p21 in colorectal cancer, DAPK2 in ovarian cancer); Promotion of proliferation and cell cycle transition (affecting expression of CDK4, CDK6, CyclinD1, c-myc); Downregulation of apoptosis mediators; Regulation of cell invasion and migration pathways

03

Biological functions

Cell proliferationCell cycle regulationCell invasionApoptosis regulationChemoresistanceEpithelial–mesenchymal transition (EMT)Stem cell phenotype regulation
04

Disease associations

CancerChemoresistanceTumor progressionMetastasisOvarian cancerColorectal cancerBrain tumors (notably embryonal tumors with multilayered rosettes, ETMR)
05

Safety considerations

No approved direct inhibitors; therapeutic targeting must avoid global miRNA dysregulationPotential for broad off-target effects due to multiple gene targetsTumor-specific upregulation—systemic modulation could impact normal tissue stem/progenitor populations
06

Interacting drugs

5-fluorouracil (5-FU)

3 more in the full profile.

07

Biomarkers

Elevated miR-520g expression (indicator of chemoresistance in ovarian and colorectal cancer)miR-520g levels (prognostic marker for poor survival in chemotherapy-treated ovarian cancer)Reduction in DAPK2 or p21 expression (surrogate downstream markers)

Beyond the preview

Go deeper on MicroRNA 520g (miR-520g).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on MicroRNA 520g (miR-520g).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call