Related Experiment Video

Updated: Apr 30, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

18.2K

Imipramine Targets Apoptosis, Metastasis, and EGFR/SRC-mediated EMT in Oral Cancer Cells

Wei-Chun Wang1,2, Ying-Tzu Chen3, Fei-Ting Hsu4

  • 1Department of Oral and Maxillofacial Surgery, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.

Anticancer Research
|April 28, 2026
PubMed
Abstract

Insights

Imipramine, an antidepressant, shows potent anticancer effects against oral cancer (OC) by inducing cell death and inhibiting metastasis. This study supports imipramine

Area of Science:

  • Pharmacology and Cancer Therapeutics
  • Molecular Oncology
  • Drug Repurposing

Background:

  • Oral cancer (OC) is aggressive with high metastatic potential.
  • Imipramine, a tricyclic antidepressant, has emerging anticancer properties.
  • Understanding imipramine's mechanisms in OC is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the therapeutic effects of imipramine on oral cancer cells.
  • To elucidate the anti-progression mechanisms of imipramine in oral cancer.

Main Methods:

  • Oral cancer cell lines (SAS, MOC1) treated with imipramine.
  • Assays included MTT for cytotoxicity, flow cytometry for apoptosis, Transwell for migration/invasion, and Western blotting for protein expression.
  • Key pathways and proteins involved in apoptosis, metastasis, and epithelial-mesenchymal transition (EMT) were analyzed.

Main Results:

  • Imipramine significantly reduced oral cancer cell viability and induced apoptosis via extrinsic and intrinsic pathways.
  • It downregulated anti-apoptotic proteins (XIAP, c-FLIP) and proliferation regulator (Cyclin D1).
  • Imipramine inhibited migration, invasion, MMP-2, MMP-9, VEGF-A, and suppressed EMT by altering key transcription factors and adhesion molecules, inactivating the EGFR/SRC axis.

Conclusions:

  • Imipramine demonstrates significant anti-oral cancer activity.
  • Mechanisms include apoptosis induction, metastasis inhibition, and EMT suppression.
  • Imipramine shows potential as a repurposed therapeutic agent for oral cancer.
Keywords:
EGFR/SRCEMTOral cancerapoptosisimipramine

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

10.8K
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

13.1K

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.3K
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...
7.0K
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.4K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
81