Related Experiment Video

Updated: Aug 16, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

1.6K

HRK inhibits colorectal cancer cells proliferation by suppressing the PI3K/AKT/mTOR pathway

Haowei Wang1,2, Yujia Chen1, Qinzi Yuan1

  • 1Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.

Frontiers in Oncology
|December 26, 2022
PubMed
Abstract

Insights

Hark protein (HRK) is underexpressed in colorectal cancer (CRC). Restoring HRK inhibits CRC cell growth and migration by suppressing the PI3K/AKT/mTOR pathway, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Colorectal cancer (CRC) is a prevalent malignancy with high mortality.
  • The BCL-2 family protein HRK exhibits antitumor properties in prostate cancer, but its role in CRC is unexplored.

Purpose of the Study:

  • To investigate the expression levels and functional role of HRK in colorectal cancer.
  • To elucidate the underlying molecular mechanisms, including the PI3K/AKT/mTOR signaling pathway.

Main Methods:

  • Analysis of HRK expression in CRC tissues and cell lines using public databases, immunohistochemistry, qPCR, and Western blotting.
  • Functional assays including proliferation, invasion, migration, colony formation, and apoptosis.
  • Rescue experiments with rapamycin to assess the PI3K/AKT/mTOR pathway's role.

Main Results:

  • HRK expression is significantly lower in CRC tissues and cell lines compared to normal counterparts.
  • Overexpression of HRK suppressed CRC cell proliferation, invasion, and migration.
  • Reduced HRK expression led to decreased apoptosis and activation of the PI3K/AKT/mTOR pathway.

Conclusions:

  • HRK is downregulated in colorectal cancer.
  • HRK functions as a tumor suppressor by inhibiting proliferation and invasion and promoting apoptosis via the PI3K/AKT/mTOR pathway.
  • HRK is a potential therapeutic target for colorectal cancer treatment.
Keywords:
CRCHRKapoptosismTORproliferationrapamycin

More Related Videos

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.8K
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.0K

Related Concept Videos

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
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...
4.9K
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...
3.9K
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.4K
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...
6.6K
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