Related Experiment Video

Updated: Jun 8, 2025

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

1.5K

Anti-Proliferation Effect of Nodosin on Hepatocellular Carcinoma Cells Via The ERCC6L/PI3K/AKT/Axis

Qingling Wang1, Qingquan Gong1, Chun Zhang1

  • 1Department of General Surgery, Mindong Hospital Affiliated to Fujian Medical University, Ningde, Fujian, China.

Journal of Biochemical and Molecular Toxicology
|November 6, 2024
PubMed

Insights

Nodosin, a diterpenoid, inhibits hepatocellular carcinoma (HCC) cell viability by downregulating ERCC6L, impacting the ERCC6L/PI3K/AKT pathway. This reveals a novel mechanism for nodosin

Area of Science:

  • Natural Products Chemistry
  • Molecular Oncology
  • Cancer Biology

Background:

  • Nodosin, a diterpenoid from Rabdosia serra, shows antitumor properties.
  • Its specific mechanism in hepatocellular carcinoma (HCC) requires elucidation for clinical use.

Purpose of the Study:

  • To investigate the molecular mechanism of nodosin's anti-HCC effects.
  • To identify key pathways regulated by nodosin in HCC cells.

Main Methods:

  • Cell viability assays (CCK8, flow cytometry) on HCC cell lines (SNU378, HCCLM3).
  • Western blot analysis to assess PI3K/AKT signaling pathway.
  • Gene manipulation (overexpression) to validate target interactions.

Main Results:

  • Nodosin significantly reduced HCC cell viability (IC50 values provided).
  • Nodosin downregulated ERCC6L expression in HCC cells.
  • ERCC6L overexpression reversed nodosin's anti-proliferative and pro-apoptotic effects.
  • ERCC6L modulated nodosin's impact on the PI3K/AKT pathway.

Conclusions:

  • Nodosin exerts anti-proliferation effects on HCC cells via the ERCC6L/PI3K/AKT axis.
  • ERCC6L acts as a key mediator in nodosin's anti-cancer activity.
  • Findings provide insights into nodosin's therapeutic potential for HCC.
Keywords:
ERCC6LPI3K/AKT signalingRabdosia serra [Maxim] Haracell apoptosiscell proliferation

More Related Videos

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds13:34

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds

Published on: April 6, 2016

10.2K
Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

5.9K

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...
3.4K
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...
3.7K
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...
4.5K
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...
4.7K
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...
6.2K