Related Experiment Video

Updated: Feb 4, 2026

Exosomal miRNA Analysis in Non-small Cell Lung Cancer NSCLC Patients' Plasma Through qPCR: A Feasible Liquid Biopsy Tool
08:49

Exosomal miRNA Analysis in Non-small Cell Lung Cancer NSCLC Patients' Plasma Through qPCR: A Feasible Liquid Biopsy Tool

Published on: May 27, 2016

11.7K

MiR-940 inhibits the progression of NSCLC by targeting FAM83F

G-M Gu1, Y-Y Zhan, K Abuduwaili

  • 1Department of Pulmonary Medicine, the Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China. liuchunlingdoc@outlook.com.

European Review for Medical and Pharmacological Sciences
|October 4, 2018
PubMed
Abstract

Insights

MicroRNA-940 (miR-940) targets family sequence similarity 83 member F (FAM83F) to inhibit non-small cell lung cancer (NSCLC) progression. Lower miR-940 levels correlate with poorer NSCLC prognosis, indicating its tumor-suppressive role.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • MicroRNA Therapeutics

Background:

  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality worldwide.
  • Identifying novel molecular targets and pathways is crucial for developing effective NSCLC therapies.
  • MicroRNAs (miRNAs) play significant roles in cancer development and progression by regulating gene expression.

Purpose of the Study:

  • To investigate the potential targeting of family sequence similarity 83 member F (FAM83F) by miR-940.
  • To determine the role of the miR-940/FAM83F axis in the progression of non-small cell lung cancer (NSCLC).

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to assess miR-940 and FAM83F expression in NSCLC tissues.
  • Cell viability assays (CCK-8) following miR-940 knockdown or overexpression in NSCLC cell lines.
  • RNA immunoprecipitation (RIP) and luciferase reporter gene assays to confirm the interaction between miR-940 and FAM83F.

Main Results:

  • MiR-940 expression was significantly decreased, while FAM83F expression was upregulated in NSCLC tissues compared to adjacent normal tissues.
  • Downregulation of miR-940 was associated with poorer overall survival, advanced tumor stage, and larger tumor size in NSCLC patients.
  • Knockdown of miR-940 promoted NSCLC cell proliferation, whereas its overexpression inhibited proliferation.
  • Direct binding of miR-940 to FAM83F was confirmed, leading to reduced FAM83F activity.

Conclusions:

  • MiR-940 acts as a tumor suppressor in NSCLC by targeting FAM83F.
  • The miR-940/FAM83F pathway represents a potential therapeutic target for NSCLC treatment.
  • Restoring miR-940 expression may offer a novel strategy to inhibit NSCLC progression.

More Related Videos

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids08:52

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids

Published on: November 22, 2021

4.6K
Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells09:58

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells

Published on: May 2, 2017

8.1K

Related Concept Videos

Feedback Inhibition00:46

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
57.2K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.4K
Enzyme Inhibition01:30

Enzyme Inhibition

Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.
92.5K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.0K
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...
4.8K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.9K