Related Experiment Video

Updated: Apr 14, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.5K

Sirtuin 3 inhibits hepatocellular carcinoma growth through the glycogen synthase kinase-3β/BCL2-associated X

C-L Song1, H Tang1, L-K Ran1

  • 1The Second Affiliated Hospital and the Key Laboratory of Molecular Biology of Infectious Diseases Designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.

Oncogene
|April 28, 2015
PubMed

Insights

Sirtuin 3 (SIRT3) suppresses liver cancer growth by activating the GSK-3β/Bax pathway, leading to apoptosis. Restoring SIRT3 may offer a new therapeutic strategy for hepatocellular carcinoma (HCC).

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Sirtuin 3 (SIRT3), a class III histone deacetylase, is linked to various cancers.
  • The specific role of SIRT3 in hepatocellular carcinoma (HCC) pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the function and mechanism of SIRT3 in hepatocellular carcinoma (HCC).
  • To explore the potential of targeting the SIRT3 pathway for HCC therapy.

Main Methods:

  • Analysis of SIRT3 expression in HCC tissues.
  • In vitro studies involving ectopic SIRT3 expression and SIRT3 depletion in HCC cells and immortalized hepatocytes.
  • Mechanistic investigations using GSK-3β inhibitors and BAX gene silencing.
  • In vivo tumor growth assays.

Main Results:

  • SIRT3 expression is frequently downregulated in HCC, correlating with tumor grade and size.
  • SIRT3 overexpression inhibits HCC cell growth and induces apoptosis.
  • SIRT3 depletion promotes cell proliferation and reduces epirubicin-induced apoptosis in hepatocytes.
  • SIRT3 activates GSK-3β, leading to increased Bax expression and mitochondrial translocation, promoting apoptosis.
  • GSK-3β inhibition or BAX silencing reverses SIRT3's effects on growth and apoptosis.
  • SIRT3 overexpression suppresses HCC tumor growth in vivo.

Conclusions:

  • SIRT3 functions as a tumor suppressor in HCC.
  • The SIRT3/GSK-3β/Bax signaling pathway is crucial for suppressing HCC growth.
  • Targeting this pathway presents a potential therapeutic strategy for HCC.

More Related Videos

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

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

Published on: December 27, 2016

9.2K

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.5K
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
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...
5.1K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
14.1K
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...
11.0K
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...
6.2K