Related Experiment Video

Updated: Aug 17, 2025

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

8.7K

The RNA-binding protein CSTF2 regulates BAD to inhibit apoptosis in glioblastoma

Yang Xu1, Fanen Yuan1, Qian Sun1

  • 1Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan University, 238 Jiefang Street, Wuhan, Hubei 430060, People's Republic of China; Central Laboratory, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, People's Republic of China.

International Journal of Biological Macromolecules
|December 15, 2022
PubMed

Insights

CSTF2 is upregulated in glioblastoma (GBM), promoting cancer cell survival by destabilizing BAD protein mRNA. Reducing CSTF2 induces GBM cell apoptosis, suggesting CSTF2 as a potential therapeutic target for GBM.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • RNA-binding proteins (RBPs) regulate gene expression in cancer.
  • CSTF2 is implicated in mRNA processing, but its role in glioblastoma (GBM) is unclear.

Purpose of the Study:

  • To investigate the role and mechanism of CSTF2 in human glioblastoma (GBM).
  • To determine if CSTF2 expression correlates with GBM prognosis and cell survival.

Main Methods:

  • Upregulation of CSTF2 in GBM tissues and cell lines.
  • In vitro and in vivo knockdown of CSTF2.
  • Analysis of CSTF2's effect on BAD protein mRNA stability and 3' UTR.
  • Correlation of CSTF2 expression with patient prognosis.

Main Results:

  • CSTF2 was found to be upregulated in GBM, correlating with poor prognosis.
  • Knockdown of CSTF2 induced apoptosis in GBM cells both in vitro and in vivo.
  • CSTF2 destabilizes BAD protein mRNA by shortening its 3' UTR, leading to decreased BAD expression.
  • Increased CSTF2 expression inhibits BAD-mediated apoptosis, promoting GBM cell survival.

Conclusions:

  • CSTF2 promotes GBM cell survival by negatively regulating BAD-mediated apoptosis.
  • CSTF2's mechanism involves binding to BAD mRNA, shortening its 3' UTR, and reducing BAD protein levels.
  • CSTF2 represents a potential therapeutic target for glioblastoma treatment.
Keywords:
ApoptosisBADCSTF2GlioblastomaRNA binding protein

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

18.8K
Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.0K

Related Concept Videos

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...
6.7K
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...
4.6K
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...
6.5K
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...
12.6K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.5K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.6K