Related Experiment Video

Updated: Sep 30, 2026

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

MsrB3 deficiency induces cancer cell apoptosis through p53-independent and ER stress-dependent pathways

Geun-Hee Kwak1, Hwa-Young Kim1

  • 1Department of Biochemistry and Molecular Biology, Yeungnam University College of Medicine, Daegu, Republic of Korea.

Archives of Biochemistry and Biophysics
|April 9, 2017
PubMed

Insights

Down-regulating methionine sulfoxide reductase B3 (MsrB3) triggers cancer cell death by inducing endoplasmic reticulum (ER) stress, independent of p53. Restoring MsrB3 levels alleviates ER stress and improves cell viability.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Stress Response

Background:

  • Methionine sulfoxide reductase B3 (MsrB3) down-regulation previously shown to induce cancer cell apoptosis via the intrinsic mitochondrial pathway.
  • The precise mechanism of MsrB3 deficiency-induced cancer cell death remains unclear.

Purpose of the Study:

  • To investigate the roles of p53 and endoplasmic reticulum (ER) stress in MsrB3 deficiency-induced cancer cell apoptosis.
  • To elucidate the molecular mechanisms linking MsrB3 depletion to cancer cell death.

Main Methods:

  • Utilized breast and colon cancer cell lines with MsrB3 depletion.
  • Assessed p53 levels, cell viability, ER stress markers, cytosolic calcium levels, and Bim activation.
  • Investigated the effect of MsrB3 overexpression in depleted cells.

Main Results:

  • MsrB3 depletion caused p53 down-regulation post-transcriptionally but induced apoptosis independently of p53 status.
  • MsrB3 deficiency significantly increased ER stress and activated the pro-apoptotic molecule Bim.
  • Elevated cytosolic calcium levels and disturbed ER calcium homeostasis were observed upon MsrB3 depletion.
  • MsrB3 re-expression mitigated ER stress and partially restored cell viability.

Conclusions:

  • MsrB3 plays a crucial role in regulating cancer cell apoptosis.
  • MsrB3 deficiency-induced apoptosis is primarily mediated by the induction of ER stress and subsequent Bim activation.
  • Maintaining ER calcium homeostasis is critical and influenced by MsrB3 levels.
Keywords:
Calcium homeostasisCancerER stressMethionine sulfoxideMsrB3p53

More Related Videos

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Related Concept Videos

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 daughter...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...