Related Experiment Video

Updated: Mar 26, 2026

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
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Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

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Knockdown of CLIC4 enhances ATP-induced HN4 cell apoptosis through mitochondrial and endoplasmic reticulum pathways

Haowei Xue1, Jinsen Lu2, Renxiang Yuan2

  • 1Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022 Anhui China.

Cell & Bioscience
|January 28, 2016
PubMed
Abstract

Insights

Chloride intracellular channel 4 (CLIC4) knockdown promotes apoptosis in head and neck squamous carcinoma cells. This suggests CLIC4 is a potential therapeutic target for treating this prevalent cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Human head and neck squamous carcinoma is a globally prevalent cancer with suboptimal clinical outcomes.
  • Chloride intracellular channel 4 (CLIC4) is implicated in cancer cell apoptosis and differentiation.
  • CLIC4's role in head and neck squamous carcinoma cell apoptosis requires further investigation.

Purpose of the Study:

  • To investigate the functional role of CLIC4 in the apoptosis of human head and neck squamous carcinoma HN4 cells.
  • To determine if CLIC4 expression levels correlate with oral squamous carcinoma.
  • To explore the mechanisms underlying CLIC4's influence on apoptosis.

Main Methods:

  • Immunohistochemical staining to assess CLIC4 expression in oral squamous carcinoma tissues.
  • CLIC4 knockdown using small interfering RNA (siRNA) in HN4 cells.
  • Analysis of apoptosis-related protein expression (Bax, Bcl-2, caspase 3, caspase 4, CHOP) and assays including TUNEL, mitochondrial membrane potential, and intracellular calcium levels.

Main Results:

  • CLIC4 expression was elevated in oral squamous carcinoma tissues compared to healthy gingival tissues.
  • CLIC4 knockdown significantly increased pro-apoptotic markers (Bax, active caspase 3, active caspase 4, CHOP) and decreased anti-apoptotic marker (Bcl-2) in HN4 cells.
  • CLIC4 suppression enhanced ATP-induced apoptosis, mitochondrial depolarization, and intracellular calcium release in HN4 cells, involving both mitochondrial and endoplasmic reticulum stress pathways.

Conclusions:

  • CLIC4 knockdown potentiates adenosine triphosphate (ATP)-induced apoptosis in head and neck squamous carcinoma HN4 cells.
  • Mitochondrial and endoplasmic reticulum stress pathways are integral to CLIC4-mediated apoptosis.
  • CLIC4 represents a promising therapeutic target for head and neck squamous carcinoma treatment.
Keywords:
Adenosine triphosphateApoptosisChloride intracellular channel 4Endoplasmic reticulum stressHead and neck squamous carcinomaMitochondrial membrane potential

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