Related Experiment Video

Updated: Jul 2, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Mitochondrially targeted wild-type p53 induces apoptosis in a solid human tumor xenograft model

Gustavo Palacios1, Howard C Crawford, Angelina Vaseva

  • 1Department of Pathology, Stony Brook University, Stony Brook, New York 11794, USA.

Cell Cycle (Georgetown, Tex.)
|August 23, 2008
PubMed

Insights

Mitochondrially targeted p53 (mitop53) delivered via adenovirus effectively kills colon cancer cells. This novel cancer therapy approach shows promise for inducing tumor cell death through apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • The tumor suppressor protein p53 has well-characterized roles in cancer, with novel functions continually being discovered.
  • Previous research demonstrated the efficacy of ex vivo retroviral transfer of mitochondrially targeted wild type p53 (mitop53) in inducing tumor cell killing in a mouse lymphoma model.

Purpose of the Study:

  • To explore the therapeutic potential of mitop53 for its pro-apoptotic effect in solid tumors.
  • To generate replication-deficient recombinant human Adenovirus type 5 (Ad5) vectors for delivering mitop53.

Main Methods:

  • Adenoviral delivery of mitop53 via intratumoral injection into HCT116 human colon carcinoma xenograft tumors in nude mice.
  • Assessment of tumor cell death and apoptotic effects in vivo and in vitro using Ad5-mitop53.

Main Results:

  • Adenoviral delivery of mitop53 demonstrated significant tumor cell death in HCT116 xenografts.
  • The apoptotic effects induced by Ad5-mitop53 were comparable in potency to conventional p53.
  • Ad5-mitop53 mediated cell death was confirmed in HCT116 cells in culture.

Conclusions:

  • Adenoviral delivery of mitop53 is an effective strategy for inducing apoptosis in solid tumors.
  • Novel mitop53 proteins hold promise for cancer therapy by leveraging p53 death signaling pathways.

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

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

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 daughter...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...