LINC01272 Suppressed Cell Multiplication and Induced Apoptosis Via Regulating MiR-7-5p/CRLS1 Axis in Lung Cancer

Related Experiment Video

Updated: Nov 2, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.8K

Xuan Ma1, Yang Liu1, Hao Tian1

  • 1Cancer Surgery Center, the Second People's Hospital of China Three Gorges University, No. 4 Tiyuchang Road, Yichang, Hubei Province 443000, P.R. China.

Journal of Microbiology and Biotechnology
|June 8, 2021
PubMed

Insights

Long non-coding RNA LINC01272 suppresses lung cancer cell growth and promotes apoptosis. It functions by regulating the miR-7-5p/CRLS1 axis, offering potential as a therapeutic target for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Long non-coding RNA (lncRNA) LINC01272 is implicated as a biomarker in various diseases, including lung squamous cell carcinoma.
  • Its specific role and underlying mechanisms in lung cancer (LC) progression require further elucidation.

Purpose of the Study:

  • To investigate the functional role and molecular mechanism of LINC01272 in lung cancer.
  • To determine the relationship between LINC01272, miR-7-5p, and cardiolipin synthase 1 (CRLS1) in lung cancer cells.

Main Methods:

  • Analysis of LINC01272 expression and prognostic value using TCGA-LUAD and Kaplan-Meier Plotter databases.
  • In vitro experiments involving transfection of LINC01272 overexpression plasmid and miR-7-5p mimic into lung cancer cell lines (A549 and PC-9).
  • Quantitative reverse transcription-polymerase chain reaction, MTT assay, cell formation assay, flow cytometry, dual luciferase reporter assay, and western blot analysis were employed.

Main Results:

  • LINC01272 was found to be downregulated in lung cancer, with low expression correlating with poor prognosis.
  • Overexpression of LINC01272 inhibited cell viability and multiplication while inducing apoptosis in lung cancer cells.
  • LINC01272 negatively regulated miR-7-5p, and CRLS1 was identified as a direct target of miR-7-5p. MiR-7-5p reversed the effects of LINC01272.

Conclusions:

  • LINC01272 suppresses lung cancer cell proliferation and induces apoptosis through the regulation of the miR-7-5p/CRLS1 axis.
  • LINC01272 acts as a tumor suppressor in lung cancer, highlighting its potential as a therapeutic target.
Keywords:
LINC01272apoptosislung cancermiR-7-5p/CRLS1multiplication

More Related Videos

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells09:45

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

8.6K
The Soft Agar Colony Formation Assay08:01

The Soft Agar Colony Formation Assay

Published on: October 27, 2014

112.7K

Related Concept Videos

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...
3.3K
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...
22.6K
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...
4.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.2K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.3K