Related Experiment Video

Updated: Apr 16, 2026

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

10.9K

Overexpression of a Novel Tumor Metastasis Suppressor Gene TMSG1/LASS2 Induces Apoptosis via a Caspase-dependent

Jing Su1, Wenjuan Yu2, Miaozi Gong3

  • 1Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.

Journal of Cellular Biochemistry
|March 5, 2015
PubMed

Insights

The tumor metastasis suppressor gene 1 (TMSG1/LASS2) inhibits cancer cell proliferation and promotes apoptosis. This study reveals TMSG1/LASS2

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The tumor metastasis suppressor gene 1 (TMSG1), also known as longevity assurance homologue 2 of yeast LAG1 (LASS2), is identified as a novel metastasis suppressor.
  • While its role in metastasis is suggested, the precise biological functions of TMSG1/LASS2 remain largely uncharacterized.

Purpose of the Study:

  • To investigate the impact of TMSG1/LASS2 protein on apoptosis and proliferation in human embryonic kidney cell lines (HEK293 and 293T).
  • To elucidate the underlying molecular mechanisms by which TMSG1/LASS2 influences these cellular processes.

Main Methods:

  • HEK293 and 293T cells were transfected with TMSG1/LASS2 expression plasmids or vector controls.
  • Cell proliferation was assessed using MTT assays.
  • Apoptosis was evaluated through morphological observations and Annexin V/propidium iodide staining via flow cytometry.
  • Protein expression levels of apoptosis-related factors (Bcl-2, cytochrome c, caspases, PARP) were analyzed by Western blot.
  • Cell cycle distribution was determined using flow cytometry.

Main Results:

  • Overexpression of TMSG1/LASS2 significantly inhibited cell proliferation in both cell lines.
  • TMSG1/LASS2 overexpression led to increased apoptosis, evidenced by morphological changes and Annexin V/PI staining.
  • Western blot analysis revealed downregulation of Bcl-2, mitochondrial release of cytochrome c, activation of procaspase-9 and procaspase-3, and PARP cleavage.
  • Cell cycle analysis indicated that TMSG1/LASS2 overexpression induced G0/G1 cell cycle arrest, contributing to inhibited proliferation.

Conclusions:

  • TMSG1/LASS2 acts as a potential tumor metastasis suppressor gene.
  • Its mechanism involves the induction of apoptosis and inhibition of cell proliferation.
  • These effects are mediated through a caspase-dependent mitochondrial pathway and G0/G1 cell cycle arrest.
Keywords:
APOPTOSISCASPASEPROLIFERATIONTMSG1/LASS2TUMOR METASTASIS

More Related Videos

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

3.8K
TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing07:05

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

6.0K

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.4K
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...
9.3K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
17.2K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
14.7K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
5.1K
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
13.8K