Related Experiment Video

Updated: Feb 16, 2026

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

7.3K

[Notch1 Gene Silenced by RNAi Inhibits Oncogenicity of Myeloma Cell Line]

Mei-Ling Li1, Mei-Qiong Chen2, Peng Zhang2

  • 1Department of Hematology, The Affiliated Zhongshan Hospital of Xiamen University, Xiamen 361004, Fujian Province, China; Department of Hematology, The Third Hospital of Guizhou Medical University, Duyun 558000, Guizhou Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|December 22, 2017
PubMed
Abstract

Insights

Notch1 gene silencing significantly inhibited multiple myeloma cell oncogenicity in mice. This approach reduced tumor growth and may offer a new treatment strategy by lowering IL-6 and VEGF levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Multiple myeloma is a hematological malignancy characterized by uncontrolled proliferation of plasma cells.
  • The Notch1 signaling pathway plays a role in cell growth and survival, and its dysregulation is implicated in various cancers.
  • Investigating novel therapeutic targets for multiple myeloma is crucial for improving patient outcomes.

Purpose of the Study:

  • To evaluate the impact of Notch1 gene silencing on the oncogenic potential of multiple myeloma cells.
  • To assess the therapeutic efficacy of Notch1 inhibition in a preclinical mouse model of multiple myeloma.

Main Methods:

  • Notch1 gene silencing was achieved using RNA interference (Notch1-shRNA) in RPMI8226 multiple myeloma cells.
  • These modified cells were xenografted into NOD/SCID mice to establish myeloma models.
  • Tumor growth kinetics, volume, and serum levels of Interleukin-6 (IL-6) and Vascular Endothelial Growth Factor (VEGF) were measured.

Main Results:

  • Notch1 gene silencing significantly suppressed tumor formation speed and reduced tumor volume in mice compared to controls (P<0.05).
  • Serum levels of IL-6 and VEGF were significantly decreased in tumor-bearing mice following Notch1 silencing (P<0.05).

Conclusions:

  • Notch1 gene silencing effectively inhibits the oncogenicity of multiple myeloma cells in a preclinical model.
  • The mechanism underlying this inhibition may involve the downregulation of IL-6 and VEGF.
  • Notch1 gene silencing presents a promising novel therapeutic strategy for multiple myeloma treatment.

More Related Videos

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos07:24

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

6.9K
Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells09:16

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

8.1K

Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
6.6K
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
7.8K
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...
4.1K
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...
24.3K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.5K
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...
5.3K