Related Experiment Video

Updated: Sep 18, 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

1.7K

Targeting Stearoyl-CoA Desaturase 1 Through PI3K-AKT-mTOR Signaling in Head and Neck Squamous Cell Carcinoma

Cheng-Ming Hsu1,2,3, Ming-Yu Yang4,5, Shun-Fu Chang6

  • 1Department of Otolaryngology-Head and Neck Surgery Chiayi Chang Gung Memorial Hospital Chiayi Taiwan.

OTO Open
|June 20, 2025
PubMed
Abstract

Insights

Targeting stearoyl-coenzyme A desaturase 1 (SCD1) and the PI3K-AKT-mTOR pathway shows promise for head and neck squamous cell carcinoma (HNSCC). Inhibiting SCD1 enhances the effectiveness of mTOR-targeted therapies against HNSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Stearoyl-coenzyme A desaturase 1 (SCD1) is crucial in fatty acid metabolism and linked to cancer progression, including head and neck squamous cell carcinoma (HNSCC).
  • The phosphoinositide 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway regulates cancer cell metabolism and survival.

Purpose of the Study:

  • To investigate the interaction between SCD1 inhibition and the PI3K-AKT-mTOR pathway in HNSCC.
  • To evaluate the therapeutic potential of targeting SCD1 in HNSCC.

Main Methods:

  • Utilized four HNSCC cell lines to assess SCD1 and mTOR pathway interplay.
  • Evaluated cell viability after mTOR inhibitor treatment.
  • Examined AKT-mTOR signaling effects on SCD1 expression via pharmacological inhibition and gene silencing.
  • Analyzed SCD1 knockdown impact on cancer cell proliferation and survival.

Main Results:

  • mTOR inhibitors decreased HNSCC cell viability and SCD1 expression.
  • AKT inhibition suppressed SCD1 expression, indicating regulation via the PI3K-AKT-mTOR axis.
  • SCD1 silencing reduced cancer cell growth and potentiated mTOR inhibitor cytotoxicity, suggesting synergy.

Conclusions:

  • SCD1 is a downstream target of the PI3K-AKT-mTOR pathway and supports HNSCC cell survival.
  • Combined targeting of SCD1 and mTOR offers a potential therapeutic strategy for HNSCC.
  • Further research is needed to explore clinical applications of combined SCD1 and mTOR-targeted therapies.
Keywords:
PI3K‐AKT‐mTOR signalinghead and neck squamous cell carcinoma (HNSCC)lipid metabolismstearoyl‐CoA desaturase 1 (SCD1)therapeutic target

More Related Videos

Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics11:28

Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics

Published on: May 11, 2016

8.6K
Three-Dimensional 3D Tumor Spheroid Invasion Assay12:19

Three-Dimensional 3D Tumor Spheroid Invasion Assay

Published on: May 1, 2015

58.0K

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...
4.0K
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...
3.9K
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...
9.3K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.2K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.8K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.7K