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Updated: Feb 16, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
[Knockdown of CMTM3 promotes migration and invasion of PC3 cell in vitro]
1Department of Urology, Peking University People's Hospital, Beijing 100044, China.
Objective:
To investigate the change of biological characteristics after stable knockdown of CKLF-like MARVEL transmembrane domain containing 3 (CMTM3) expression in PC3 by lentivirus shRNA and to reveal new therapeutic targets.
Methods:
The research includes two groups: sh393 is the experimental group in which CMTM3 is knocked down in PC3 cell line; shN is the control group in which CMTM3 is negatively knocked down. The expression of CMTM3 was detected by Western blot. The migration ability of PC3 after stable knockdown was detected by Transwell and Wound healing assay. The invasion ability of PC3 was detected by Matrigel assay. RESULTS were obtained from at least three individual experiments.
Results:
The expression of CMTM3 in sh393 group is significant lower than shN group (0.004 0±0.000 4 vs. 0.490 0±0.055 7, P<0.001) detected by Western blot. It also had statistical significance in Matrigel assays (248.6±4.5 vs. 113.0± 3.3), Transwell (203.6±1.9 vs. 103.0±1.2) and Wound healing assays (95.0±2.9 vs. 33.0±1.5) that knockdown of CMTM3 promoted migration, and invasion of PC3 cells in vitro (P<0.001).
Conclusion:
Negative correlation exists between the stable knockdown of CMTM3 and change of biological characteristics in PC3 cells, and knocking down CMTM3 affects migration, and invasion ability in PC3 cells.
Insights
Knocking down CMTM3 in PC3 cells significantly enhances their migration and invasion abilities. This suggests CMTM3 plays a crucial role in regulating these aggressive cancer cell characteristics.
Area of Science:
- Oncology
- Molecular Biology
Background:
- The role of CKLF-like MARVEL transmembrane domain containing 3 (CMTM3) in cancer progression is not fully understood.
- Identifying key regulators of cancer cell migration and invasion is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To investigate the biological consequences of stable CMTM3 knockdown in PC3 prostate cancer cells.
- To explore CMTM3 as a potential therapeutic target for prostate cancer.
Main Methods:
- Stable knockdown of CMTM3 in PC3 cells was achieved using lentivirus-mediated shRNA.
- CMTM3 expression levels were confirmed by Western blot.
- Cell migration and invasion were assessed using Transwell, Matrigel, and Wound healing assays.
Main Results:
- Western blot confirmed significantly reduced CMTM3 expression in the knockdown group compared to controls (P<0.001).
- Knockdown of CMTM3 markedly promoted PC3 cell migration and invasion in vitro (P<0.001).
- Specific assay results showed significant increases in migration and invasion metrics post-CMTM3 knockdown.
Conclusions:
- A negative correlation exists between CMTM3 knockdown and changes in PC3 cell biological characteristics.
- Downregulation of CMTM3 enhances the migration and invasion capabilities of PC3 cells, indicating its role in cancer aggressiveness.

