Premium
siRNA Mediated Knockdown of MLF1 Gene Suppressed the Proliferation and Colony Forming Ability of Human Lung Cancer Cells.
Author(s) -
Wang Hongtao,
Yang Jin,
Zhu Guoliang,
Yan Ruxue,
Zhang Yao,
Wang Xiaojing
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.677.20
Subject(s) - a549 cell , cell cycle , biology , lung cancer , cancer research , cell growth , gene knockdown , gene silencing , flow cytometry , cell , cancer , cell culture , pathology , microbiology and biotechnology , medicine , gene , genetics
Background Lung cancer is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung. Myeloid leukemia factor 1 (MLF1) is a protein involved in myeloid cell differentiation which regulates the cell cycle and the expression of numerous genes. The role of MLF1 in hematologic cancers is well established, As yet, there is little knowledge of MLF1 expression and biological function in lung cancer. Here, we investigated the role of MLF1 in lung cancer using a variety of cell lines along with patient samples to determine whether MLF1 played a significant role in this devastating disease. Materials and Methods Lung cancer cell lines (A549, H1975, HCC827, and NCI‐H460) and primary lung tissue were used to assess the relative levels of MLF1 in lung cancer. The lung cancer cell line A549 was lentivirally transfected to silence endogenous MLF1 gene expression, which was confirmed by real‐time quantitative PCR (qPCR). Cell proliferation was assessed through fluorescence imaging and MTT assays. Cell cycle analysis was performed utilizing flow cytometry and formation of cell colonies evaluated microscopically. Results Proliferation of A549 cells was significantly inhibited in cells where MLF1 was silenced compared to controls. Cell cycle analysis indicated that cell cycle phases were not significantly changed upon silencing of MLF1 in lung cancer cells. A significant increase in apoptosis was observed in MLF1‐knockdown cells, while a significant decrease in number of cell colonies formed was observed in MLF1‐knockdown cells compared to controls. In most, but not all, human lung cancer tissue samples MLF1 was upregulated. Conclusion In summary, MLF1 promotes the proliferation and colony forming abilities of lung cancer cells and significantly decreases apoptosis while have no impact on cell cycle. Further studies with larger sample sizes are needed 1) to conclude whether human lung cancers upregulate MLF1, 2) to reveal the mechanism of action for MLF1 in lung carcinogenesis and 3) investigate MLF1 gene therapy for the treatment of lung cancer. Support or Funding Information This work was supported by Key Program of Natural Science Research of Higher Education of Anhui Province (Grant KJ2016A472 KJ2017A241), Key program for excellent young talents in college and university of Anhui province (Grant gxyqZD2016168), National Natural Science Foundation of China (Grant 81772493), and College students' innovation and entrepreneurship training project (Grant 201610367007) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .