Related Experiment Video

Updated: Aug 16, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

RNA interference against Hec1 inhibits tumor growth in vivo

E N Gurzov1, M Izquierdo

  • 1Department of Molecular Biology, Centro de Biología Molecular 'Severo Ochoa', Universidad Autónoma de Madrid, Facultad de Ciencias, Cantoblanco, Madrid, Spain.

Gene Therapy
|August 27, 2005
PubMed

Insights

Targeting Hec1 (highly expressed in cancer) protein synthesis with shRNAs disrupts cancer cell division and reduces tumor size. This approach shows promise for developing new anti-cancer therapies by blocking cell proliferation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Hec1 (highly expressed in cancer) is crucial for accurate chromosome segregation during cell division.
  • Proper chromosome alignment and spindle attachment are monitored by checkpoint proteins interacting with Hec1.

Purpose of the Study:

  • To investigate the potential of inhibiting Hec1 synthesis as a strategy to disrupt tumor cell division.
  • To evaluate the efficacy of Hec1 depletion in reducing tumor growth in vitro and in vivo.

Main Methods:

  • Utilized retrovirus and adenovirus vectors to deliver short hairpin RNAs (shRNAs) targeting Hec1 synthesis.
  • Assessed Hec1 protein depletion, cellular arrest, and mitotic catastrophe in HeLa and U-373-MG cancer cell lines.
  • Evaluated tumor size reduction in nude mice bearing induced adenocarcinomas treated with Hec1-shRNA vectors.

Main Results:

  • Vector-expressed shRNAs achieved highly efficient depletion of Hec1 protein.
  • Significant cellular arrest and mitotic catastrophe were observed in cancer cell lines 96 hours post-infection.
  • Adenocarcinomas in mice treated with Hec1-shRNA vectors showed a significant reduction in size compared to controls.

Conclusions:

  • Depletion of Hec1 effectively inhibits cell division and induces mitotic catastrophe in cancer cells.
  • Targeting Hec1 represents a viable new strategy for blocking proliferating tumor cells.
  • Hec1 inhibition demonstrates potential as an anti-cancer therapeutic approach.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

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...
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 daughter...
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...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...