Related Experiment Video

Updated: Nov 5, 2025

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.2K

KIF4A knockdown suppresses ovarian cancer cell proliferation and induces apoptosis by downregulating BUB1 expression

Wumin Jin1, Lianmin Ye2

  • 1Reproductive Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

Molecular Medicine Reports
|May 20, 2021
PubMed

Insights

Kinesin family member 4A (KIF4A) promotes ovarian cancer progression by regulating BUB1. Suppressing KIF4A inhibits cancer cell growth and migration, offering potential therapeutic targets for ovarian cancer.

Area of Science:

  • Gynecological Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Ovarian cancer is a leading cause of cancer-related deaths globally.
  • The precise molecular mechanisms driving ovarian cancer progression, particularly the role of Kinesin Family Member 4A (KIF4A), remain incompletely understood.
  • Abnormal KIF4A expression is linked to ovarian cancer advancement.

Purpose of the Study:

  • To elucidate the molecular mechanisms of KIF4A in ovarian cancer.
  • To investigate the relationship between KIF4A and Budding Uninhibited by Benzimidazoles 1 (BUB1) in ovarian cancer.
  • To assess the therapeutic potential of targeting KIF4A and BUB1.

Main Methods:

  • Quantitative PCR and Western blotting were used to measure KIF4A and BUB1 expression.
  • Cell proliferation, migration, and apoptosis were assessed using Cell Counting Kit-8, colony formation, wound healing, TUNEL, and flow cytometry assays.
  • Co-immunoprecipitation assays determined the interaction between KIF4A and BUB1.

Main Results:

  • KIF4A expression was significantly elevated in ovarian cancer cell lines compared to normal IOSE-80 cells.
  • KIF4A knockdown markedly reduced cell viability, colony formation, and migration, while inducing apoptosis.
  • KIF4A physically interacts with and regulates BUB1 expression; BUB1 overexpression counteracted the effects of KIF4A knockdown.

Conclusions:

  • KIF4A knockdown suppresses ovarian cancer progression by regulating BUB1.
  • KIF4A and BUB1 represent promising therapeutic targets for ovarian cancer treatment.
Keywords:
apoptosisbudding uninhibited by benzimidazoles 1kinesin family member 4Aovarian cancerproliferation

More Related Videos

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures07:48

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures

Published on: December 26, 2016

11.6K
Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

11.1K

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...
5.1K
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...
7.2K
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...
4.8K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.4K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.4K