Related Experiment Video

Updated: Jun 24, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

Induction of Akt activity by chemotherapy confers acquired resistance

Wei-Chien Huang1, Mien-Chie Hung

  • 1Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University and Hospital, and Department of Biotechnology, Asia University, Taichung, Taiwan. whuang@mail.cmu.edu.tw

Journal of the Formosan Medical Association = Taiwan Yi Zhi
|March 19, 2009
PubMed

Insights

Chemotherapy resistance in cancer is often linked to the PI3K/Akt pathway. Targeting this pathway with inhibitors alongside chemotherapy shows promise in overcoming drug resistance and improving cancer treatment efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Chemotherapy resistance is a primary obstacle in cancer treatment.
  • The Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/Akt) pathway is frequently activated in chemoresistant cancers.
  • Akt pathway modulation is a common feature in cancers that resist chemotherapeutic drugs.

Purpose of the Study:

  • To review the molecular mechanisms by which chemotherapeutic agents activate the PI3K/Akt pathway.
  • To discuss how activated Akt confers chemoresistance by regulating critical cellular functions.
  • To explore strategies for overcoming therapeutic resistance by targeting the PI3K/Akt pathway.

Main Methods:

  • Literature review of studies on PI3K/Akt pathway activation and chemoresistance.
  • Analysis of molecular mechanisms linking chemotherapy agents to Akt activation.
  • Evaluation of in vitro and in vivo data on PI3K/Akt inhibitors combined with chemotherapy.

Main Results:

  • Chemotherapeutic agents can activate the PI3K/Akt pathway, promoting cancer cell survival and proliferation.
  • Activated Akt confers chemoresistance by regulating protein synthesis, anti-apoptosis, and survival signaling.
  • Combination therapy with PI3K/Akt inhibitors and chemotherapy enhances treatment efficacy in preclinical models.

Conclusions:

  • Targeting the PI3K/Akt pathway is a promising strategy to overcome chemotherapy resistance.
  • Understanding regulatory mechanisms of Akt activity is crucial for developing effective anti-cancer therapies.
  • Disrupting feedback and feedforward loops in signaling networks may enhance the efficacy of PI3K/Akt-targeted treatments.

More Related Videos

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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...
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 specific...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...