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Updated: Jun 25, 2026
An In Vivo Murine Sciatic Nerve Model of Perineural Invasion
Published on: April 23, 2018
Inhibition of CD146 gene expression via RNA interference reduces in vitro perineural invasion on ACC-M cell
1Department of Oral and Maxillofacial Surgery, Fourth Military Medical University, Shaanxi, China.
Background:
Overexpression of melanoma cell adhesion molecule (MCAM or CD146), a novel member of the immunoglobulin gene superfamily, promotes invasion, metastasis, growth and survival of malignant cells.
Materials And Methods:
Here, we used a human U6 promoter-driven DNA template approach to induce short hairpin RNA (shRNA)-triggered RNA interference to block CD146 gene expression in the human high-metastatic adenoid cystic carcinoma (ACC) cell line ACC-M. reverse transcription-polymerase chain reaction, Western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assay, flow cytometry analysis and in vitro perineural invasion (PNI) assay were used to investigate the effects of CD146 on cell growth, cell cycle distribution and cell PNI activity in ACC-M cells.
Results:
We have demonstrated that different shRNAs can specifically knockdown the transcription of CD146, resulting in the inhibition of cell proliferation, and G(0)/G(1) to S phase arrest in ACC-M cells. Knockdown of CD146 by shRNA resulted in decrease of the ACC-M PNI activity in vitro.
Conclusion:
These findings suggested that CD146 was an ACC-related gene and CD146 may play an important role in the carcinogenesis, progression and PNI activity of ACC.
Insights
Melanoma cell adhesion molecule (MCAM) knockdown inhibits adenoid cystic carcinoma (ACC) cell growth and perineural invasion. Targeting CD146 may be a therapeutic strategy for ACC progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Melanoma cell adhesion molecule (MCAM), also known as CD146, is an immunoglobulin superfamily member.
- MCAM/CD146 overexpression is linked to enhanced invasion, metastasis, growth, and survival in malignant cells.
Purpose of the Study:
- To investigate the role of CD146 in adenoid cystic carcinoma (ACC) using RNA interference.
- To assess the impact of CD146 gene silencing on ACC cell proliferation, cell cycle, and perineural invasion (PNI).
Main Methods:
- Utilized a human U6 promoter-driven DNA template for short hairpin RNA (shRNA)-mediated CD146 gene silencing in ACC-M cells.
- Employed reverse transcription-polymerase chain reaction (RT-PCR) and Western blot to confirm CD146 knockdown.
- Assessed cell proliferation (MTT assay), cell cycle distribution (flow cytometry), and in vitro PNI activity.
Main Results:
- Specific shRNAs effectively reduced CD146 transcription and protein levels in ACC-M cells.
- CD146 knockdown inhibited ACC cell proliferation and induced G0/G1 to S phase arrest.
- Silencing CD146 significantly decreased the in vitro PNI activity of ACC-M cells.
Conclusions:
- CD146 is implicated as an ACC-related gene.
- CD146 plays a crucial role in ACC carcinogenesis, progression, and perineural invasion.
- Targeting CD146 presents a potential therapeutic avenue for managing ACC.
