Related Experiment Video

Updated: Apr 26, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

18.2K

miR-101 promotes breast cancer cell apoptosis by targeting Janus kinase 2

Lu Wang1, Linqiang Li, Rui Guo

  • 1Department of Pharmacology (State-Province Key Laboratories of Biomedicine- Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin, P. R.China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|July 26, 2014
PubMed
Abstract

Insights

microRNA-101 (miR-101) is reduced in breast cancer. Restoring miR-101 inhibits cancer cell growth and promotes apoptosis by targeting Janus kinase 2 (Jak2), suggesting miR-101 as a potential breast cancer therapy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • microRNA-101 (miR-101) is frequently downregulated in various cancers.
  • Understanding the role of miR-101 in breast cancer is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional impact of dysregulated miR-101 on breast cancer cells.
  • To elucidate the molecular mechanisms underlying miR-101's effects in breast cancer.

Main Methods:

  • Quantification of miR-101 levels using real-time RT-PCR.
  • Assessment of cell viability via MTT assay.
  • Detection of apoptosis using flow cytometry and TUNEL assay.
  • Determination of protein expression by Western blot.

Main Results:

  • miR-101 levels were significantly decreased in human breast cancer tissues and cell lines.
  • Overexpression of miR-101 suppressed proliferation and induced apoptosis in breast cancer cells.
  • Janus kinase 2 (Jak2) was identified as a direct target of miR-101, and its knockdown promoted apoptosis.
  • A negative correlation was observed between miR-101 and Jak2 levels in breast cancer samples.

Conclusions:

  • miR-101 inhibits breast cancer cell proliferation and promotes apoptosis through the targeting of Jak2.
  • Modulating miR-101 expression presents a promising therapeutic avenue for breast cancer treatment.

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

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

Published on: June 9, 2023

2.3K
Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

12.4K

Related Concept Videos

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...
6.2K
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...
3.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.5K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.0K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
20.9K
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...
10.1K