The knockdown of c-myc expression by RNAi inhibits cell proliferation in human colon cancer HT-29 cells in vitro and in vivo
Open accessAbstract
We investigated the effects of RNA interference-mediated silencing of the c-myc gene on celluar proliferation and apoptosis in human colon cancer HT-29 cells in vitro and in vivo. A small interfering RNA (siRNA) targeting c-myc was designed, the DNA template was synthesized, and the siRNA was obtained by in vitro transcription. After siRNA transfection into HT-29 and human neuroblastoma IMR-32 cells with Lipofectamine 2000™, the proliferation of the HT-29 and IMR-32 cells was assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and Hoechst 33258 staining was used to observe cell apoptosis. Following gene transfer to HT-29 cells, the expression of c-myc mRNA was examined via reverse transcription polymerase chain reaction, and the level of the protein via Western blot assay. Growth curves were constructed and in vivo experiments were performed on nude mice to assess the effects of c-myc silencing on tumor growth. The c-myc expression in the tumor tissue was measured by reverse transcription polymerase chain reaction and subsequently by immunohistochemistry. Our paper demonstrates that the delivery of siRNA directed against c-myc not only efficiently down-regulated the expression of c-myc, inhibited the proliferation of HT-29 cells and induced apoptosis in vitro, but also suppressed the growth of colon cancer cells in vivo.
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Ge's c-Myc siRNA down-regulated c-Myc expression, inhibited cell proliferation, induced apoptosis in HT-29 cells in vitro, and suppressed colon cancer cell growth in vivo.
“This resulted in down-regulation of c-Myc expression, inhibition of cell proliferation, and induction of apoptosis in vitro. Furthermore, the growth of colon cancer cells was suppressed in vivo.576”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [576]
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Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials
Xie, X., Yu, T., Li, X., Zhang, N., Foster, L. J., Peng, C., Huang, W., & He, G. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01589-z · Cited by 396 · see citing works
- Authors
- Zhang, X., Ge, Y.-L., & Tian, R.-H.
- Affiliations
- Qingdao University (CN)
- ORCID
- Zhang, Xiao
- Venue
- Cellular and Molecular Biology Letters
- Publisher
- Walter de Gruyter GmbH
- Published
- 2009-01-01
- Volume
- 14
- Issue
- 2
- Pages
- 305-18
- ISSN
- 1425-8153 (ISSN-L)
- 1689-1392
- PMC
- PMC6275647
- OpenAlex
- W2036032768
- Cited by
- 55
- References
- 28
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 1 · 2021: 7 · 2020: 7 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 1 · 2013: 3 · 2012: 4
- FWCI
- 2.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (tdm)
- Locations
- Cellular & Molecular Biology Letters (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- c-Myc, RNA interference, siRNA, gene silencing, colon cancer, HT-29 cells, cell proliferation, apoptosis, tumor growth inhibition, nude mouse xenograft
- MeSH terms
- Animals, Colonic Neoplasms, Female, Humans, Mice, Inbred BALB C, Neoplasm Transplantation, Transplantation, Heterologous, Proto-Oncogene Proteins c-myc, HT29 Cells, RNA Interference, Cell Proliferation, Mice, Gene Knockdown Techniques
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