Related Experiment Video

Updated: Aug 7, 2025

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

8.5K

Inhibition of CDKL3 downregulates STAT1 thus suppressing prostate cancer development

Qi Jiang1, Juan Li2, Jingyue Wang3

  • 1Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100 Haining Road, Shanghai, 200080, China.

Cell Death & Disease
|March 10, 2023
PubMed

Insights

Cyclin-dependent kinase-like 3 (CDKL3) is upregulated in prostate cancer, promoting tumor growth and migration. Inhibiting CDKL3 offers a potential new therapeutic strategy for prostate cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Prostate cancer remains a significant global health concern for men.
  • Current treatment options are limited by an incomplete understanding of prostate cancer's molecular underpinnings.
  • The role of Cyclin-dependent kinase-like 3 (CDKL3) in prostate cancer is currently unknown.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of CDKL3 in prostate cancer.
  • To determine if CDKL3 can be a potential therapeutic target for prostate cancer.

Main Methods:

  • Analysis of CDKL3 expression in prostate cancer tissues versus normal tissues.
  • In vitro studies involving CDKL3 knockdown in prostate cancer cells to assess effects on cell growth, migration, apoptosis, and cell cycle.
  • In vivo studies evaluating the tumorigenic capacity of cells with varying CDKL3 expression levels.
  • Exploration of downstream signaling pathways, including STAT1 and the ERK pathway.

Main Results:

  • CDKL3 was significantly upregulated in prostate cancer tissues and correlated positively with tumor malignancy.
  • CDKL3 knockdown inhibited prostate cancer cell growth, migration, and in vivo tumorigenicity, while enhancing apoptosis and G2 cell cycle arrest.
  • CDKL3 regulates STAT1 by inhibiting its CBL-mediated ubiquitination, and its effects are dependent on the ERK pathway and STAT1.

Conclusions:

  • CDKL3 acts as a novel prostate cancer-promoting factor.
  • CDKL3 influences prostate cancer progression through regulation of STAT1 and the ERK pathway.
  • CDKL3 represents a potential therapeutic target for prostate cancer.

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.3K
An Orthotopic Murine Model of Human Prostate Cancer Metastasis06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

35.3K

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...
4.8K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.1K
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...
4.6K
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.
35.5K
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...
3.8K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.8K