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Updated: Jan 22, 2026
Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines
Published on: September 3, 2016
Role of TMPRSS4 Modulation in Breast Cancer Cell Proliferation
Ganiou Assani1,2, Akadiri Yessoufou3, Yudi Xiong1,2
1Hubei Cancer Clinical Study Center, Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital, Wuhan University, Wuhan, China.
Abstract:
Background: TMPRSS4 is a novel Type II transmembrane serine protease found at the surface of the cells and is involved in the development and cancer progression. However, TMPRSS4 functions in breast cancer remain poor understand. The present study investigated the function of TMPRSS4 in the breast cancer cells and the potential mechanistic action underling. Materials and Methods: The lentiviral vectors causing TMPRSS4 down-regulation and over-expression were established and transfected in MDA-MB-468 and MCF-7 cells, respectively. By using the CCK- 8 assay, cell proliferation was analyzed. Moreover, western blot was used to detect the expression of certain proteins related to cell apoptosis (Bax and Bcl2) signaling pathway and telomere maintenance (POT1, TPP1, and UBE2D3). Cell cycle and cell apoptosis were also analyzed by using the Flow cytometry analysis. TMPRSS4 expression was detected at the mRNA level and protein level by performing qPCR and western blot technique, respectively. Results: TMPRSS4 expression is inhibited in stable transfected MDA-MB-468-shTMPRSS4 cells compared to the control MDA-MB-468-NC and its expression is up-regulated in stable transfected MCF-7-TMPTSS4 compared to its control MCF-7-NC. Moreover, TMPRSS4 silencing in breast cancer reduces cells proliferation by promoting cell cycle arrest in G2/M phase, cell apoptosis, and telomere maintenance impairment while the TMPRSS4 overexpression increases cells proliferation through cell apoptosis reduction and telomere maintenance reinforcement associated with insignificant change in cell cycle progression. Conclusion: TMPRSS4 plays important roles in cancer progression and may be considered as a good therapeutic target for cancer gene therapy especially breast cancer.
Insights
TMPRSS4 (Transmembrane Serine Protease 4) promotes breast cancer progression by enhancing cell proliferation and telomere maintenance. Inhibiting TMPRSS4 reduces tumor growth, suggesting it as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Transmembrane Serine Protease 4 (TMPRSS4) is implicated in cancer development and progression.
- The specific role of TMPRSS4 in breast cancer remains largely uncharacterized.
- Understanding TMPRSS4's function is crucial for developing targeted breast cancer therapies.
Purpose of the Study:
- To investigate the functional role of TMPRSS4 in breast cancer cells.
- To elucidate the underlying molecular mechanisms of TMPRSS4's action in breast cancer progression.
- To evaluate TMPRSS4 as a potential therapeutic target for breast cancer.
Main Methods:
- Established lentiviral vectors for TMPRSS4 down-regulation (shRNA) and over-expression.
- Utilized CCK-8 assay for cell proliferation analysis.
- Employed Western blot to assess apoptosis (Bax, Bcl2) and telomere maintenance proteins (POT1, TPP1, UBE2D3).
- Performed Flow cytometry for cell cycle and apoptosis analysis.
- Quantified TMPRSS4 mRNA and protein levels using qPCR and Western blot.
Main Results:
- TMPRSS4 silencing in MDA-MB-468 cells reduced proliferation, induced G2/M cell cycle arrest, promoted apoptosis, and impaired telomere maintenance.
- TMPRSS4 over-expression in MCF-7 cells increased proliferation by reducing apoptosis and reinforcing telomere maintenance, with minor cell cycle effects.
- Confirmed successful modulation of TMPRSS4 expression at both mRNA and protein levels.
Conclusions:
- TMPRSS4 significantly contributes to breast cancer progression.
- TMPRSS4 influences cell proliferation, apoptosis, cell cycle, and telomere maintenance pathways.
- TMPRSS4 represents a promising therapeutic target for breast cancer gene therapy.
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