Related Experiment Video

Updated: Aug 14, 2026

Isolation and Characterization of Tumor-initiating Cells from Sarcoma Patient-derived Xenografts
07:18

Isolation and Characterization of Tumor-initiating Cells from Sarcoma Patient-derived Xenografts

Published on: June 13, 2019

Phenotypic changes associated with DYNACTIN-2 (DCTN2) over expression characterise SJSA-1 osteosarcoma cells

Kieran L Bransfield1, Jon M Askham, Jack P Leek

  • 1Molecular Medicine Unit, The University of Leeds, St. James's University Hospital, Leeds, United Kingdom.

Molecular Carcinogenesis
|December 22, 2005
PubMed

Insights

Persistent DYNACTIN-2 (DCTN2) overexpression in cancer cells causes cellular changes but does not appear to drive carcinogenesis. Further studies are needed to confirm this finding in cancer development.

Area of Science:

  • Oncology
  • Cell Biology
  • Genetics

Background:

  • DYNACTIN-2 (DCTN2) is located on chromosome 12q13-q15, a region amplified in various cancers.
  • Transient DCTN2 overexpression disrupts the DYNEIN-dynactin motor, affecting cellular processes like cargo transport, centrosome function, and mitosis, potentially predisposing cells to cancer.

Purpose of the Study:

  • To investigate the role of DCTN2 genomic amplification and sustained overexpression in cancer cells.
  • To determine if DCTN2 overexpression contributes to carcinogenesis.

Main Methods:

  • Quantitative fluorescent multiplex PCR (QFMPCR) to analyze chromosome 12q13-q15 amplicons in cancer cell lines.
  • Western blot analysis to assess DCTN2 protein levels.
  • Microscopy to evaluate DCTN2 immunofluorescence, centrosome, and Golgi marker localization.

Main Results:

  • DCTN2 amplification was detected in SJSA-1, U373MG, and SJRH30 cells.
  • Sustained DCTN2 overexpression was observed only in SJSA-1 cells.
  • SJSA-1 cells exhibited altered DCTN2 immunofluorescence and diminished centrosome/Golgi marker focus, yet showed unimpaired TP53 nuclear transport and were easily propagated.

Conclusions:

  • Persistent DCTN2 overexpression is tolerated in SJSA-1 cancer cells despite predicted phenotypic abnormalities.
  • This preliminary study suggests DCTN2 overexpression may not play a major role in carcinogenesis.
  • Further research is required to definitively establish the role of DCTN2 in cancer development.

More Related Videos

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia08:14

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

Related Concept Videos

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...
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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Pleiotropy01:33

Pleiotropy

Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
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 until 1985...