Related Experiment Video

Updated: Mar 24, 2026

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

3.3K

HSP27 Knockdown Increases Cytoplasmic p21 and Cisplatin Sensitivity in Ovarian Carcinoma Cells

Hao Lu1, Chaoyang Sun, Ting Zhou

  • 1Cancer Biology Medical Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Oncology Research
|March 3, 2016
PubMed

Insights

Heat shock protein 27 (HSP27) promotes cisplatin resistance in ovarian cancer by activating the phosphorylated-Akt pathway, inhibiting p21 transfer. Targeting HSP27 may overcome drug resistance in ovarian tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Drug resistance is a major challenge in ovarian cancer chemotherapy.
  • The precise mechanisms underlying chemoresistance in ovarian cancer remain largely unknown.
  • Heat shock protein 27 (HSP27) is implicated in cellular stress responses.

Purpose of the Study:

  • To investigate the role of HSP27 in cisplatin resistance in ovarian cancer.
  • To elucidate the molecular mechanisms by which HSP27 contributes to chemoresistance.
  • To explore HSP27 as a potential therapeutic target for refractory ovarian tumors.

Main Methods:

  • Utilized cisplatin-resistant ovarian cancer cell lines (C13*).
  • Employed HSP27 small interfering RNA (siRNA) transfection to assess its functional role.
  • Investigated the involvement of the phosphorylated-Akt pathway and p21 cellular localization.

Main Results:

  • HSP27 protein was significantly upregulated in cisplatin-resistant ovarian cancer cells (C13*).
  • HSP27 siRNA transfection successfully reversed cisplatin resistance in C13* cells.
  • HSP27 activates the phosphorylated-Akt pathway, inhibiting p21 nuclear-to-plasma transfer, thereby conferring chemoresistance.

Conclusions:

  • HSP27 plays a critical role in mediating cisplatin resistance in ovarian cancer.
  • The mechanism involves the activation of the phosphorylated-Akt pathway and subsequent inhibition of p21 translocation.
  • HSP27 represents a promising therapeutic target for overcoming chemoresistance in ovarian cancer patients.

More Related Videos

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.5K
Enrichment for Chemoresistant Ovarian Cancer Stem Cells from Human Cell Lines11:50

Enrichment for Chemoresistant Ovarian Cancer Stem Cells from Human Cell Lines

Published on: September 10, 2014

14.0K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.2K
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...
5.4K
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...
10.4K
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...
3.3K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.8K