Related Experiment Video

Updated: Apr 5, 2026

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
08:32

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

1.4K

Novel Epigenetic CREB-miR-630 Signaling Axis Regulates Radiosensitivity in Colorectal Cancer

Yan Zhang1, Jiang Yu1, Hao Liu1

  • 1Department of General Surgery, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.

Plos One
|August 12, 2015
PubMed
Abstract

Insights

MicroRNA-630 (miR-630) enhances colorectal cancer radiosensitivity by inducing apoptosis. This pathway involves CREB, miR-630, and target genes BCL2L2 and TP53RK, offering new therapeutic targets.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • MicroRNA-630 (miR-630) is implicated in various cancers.
  • Its precise role in colorectal cancer (CRC) radioresistance is not fully understood.

Purpose of the Study:

  • To elucidate the molecular function and regulatory mechanisms of miR-630 in CRC radioresistance.
  • To identify key genes and pathways influenced by miR-630.

Main Methods:

  • Overexpression and loss-of-function studies of miR-630 in CRC cell lines.
  • Assessment of cell growth and apoptosis following ionizing radiation (IR).
  • Dual-luciferase assay, Western blot, chromatin immunoprecipitation, and demethylation experiments.

Main Results:

  • miR-630 expression positively correlates with CRC radiosensitivity.
  • miR-630 induces apoptosis post-IR, while its downregulation reduces radiosensitivity.
  • BCL2L2 and TP53RK identified as direct miR-630 targets, mediating its function.
  • CREB identified as a regulator of miR-630 levels, which can be increased by demethylation.

Conclusions:

  • A novel CREB-miR-630-BCL2L2/TP53RK signaling cascade regulates CRC radiosensitivity.
  • This pathway enhances apoptosis and cell death, presenting potential therapeutic targets.

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

14.6K
Intestinal Epithelial Regeneration in Response to Ionizing Irradiation09:10

Intestinal Epithelial Regeneration in Response to Ionizing Irradiation

Published on: July 27, 2022

2.8K

Related Concept Videos

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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
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...
6.4K
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
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
10.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

3.0K