Related Experiment Video

Updated: Jun 18, 2026

Analyzing Mitochondrial Function in a Drosophila melanogaster PINK1B9-Null Mutant Using High-resolution Respirometry
09:20

Analyzing Mitochondrial Function in a Drosophila melanogaster PINK1B9-Null Mutant Using High-resolution Respirometry

Published on: November 10, 2023

Proproliferative functions of Drosophila small mitochondrial heat shock protein 22 in human cells

Renu Wadhwa1, Jihoon Ryu2, Ran Gao1

  • 1From the National Institute of Advanced Industrial Science and Technology, Central 4, 1-1-1 Higashi, Tsukuba, Ibaraki 305 8562, Japan.

The Journal of Biological Chemistry
|December 2, 2009
PubMed

Insights

Mitochondrial Hsp22 protein slows aging in human cells and extends lifespan. However, it also enhances cancer cell malignancy and drug resistance by inactivating the p53 tumor suppressor protein.

Area of Science:

  • Cellular biology
  • Aging research
  • Molecular biology

Background:

  • Aging involves cellular damage and protein aggregation.
  • Chaperones, like small heat shock proteins, combat misfolding and aggregation.
  • Mitochondrial Hsp22 (DmHsp22) in Drosophila melanogaster is upregulated during aging and extends lifespan.

Purpose of the Study:

  • To investigate the cross-species effects of DmHsp22.
  • To determine if DmHsp22 can slow aging in human cells.
  • To assess the impact of DmHsp22 on human cancer cells.

Main Methods:

  • Expressing DmHsp22 in normal human fibroblasts and human cancer cells.
  • Measuring senescence-associated beta-galactosidase levels.
  • Evaluating cancer cell malignancy (anchorage-independent growth, tumor formation in mice).
  • Assessing drug resistance.
  • Investigating interaction with p53 tumor suppressor protein.

Main Results:

  • DmHsp22 is functionally active in human cells.
  • DmHsp22 extended the lifespan of normal fibroblasts, reducing senescence.
  • DmHsp22 increased malignancy and drug resistance in cancer cells.
  • DmHsp22 was found to interact with and inactivate wild-type p53.

Conclusions:

  • DmHsp22 can slow the aging process in human cells.
  • DmHsp22 enhances malignant properties of human cancer cells, potentially via p53 inactivation.
  • DmHsp22 has conserved functions across species, impacting both aging and cancer biology.

More Related Videos

Studying Mitochondrial Structure and Function in Drosophila Ovaries09:53

Studying Mitochondrial Structure and Function in Drosophila Ovaries

Published on: January 4, 2017

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing08:34

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Published on: September 27, 2016

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...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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...
Energy to Drive Translocation01:37

Energy to Drive Translocation

Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
Generally, polypeptides are unfolded by two distinct...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...