title: MyD88 expression is associated with paclitaxel resistance in lung cancer A549 cells.
abstract: The purpose of the present study was to investigate the relationship between myeloid differentiation primary response gene 88 (MyD88) expression and the resistance to paclitaxel of A549 lung cancer cells. In order to achieve MyD88 gene overexpression or knockdown in the A549 cell line, the cells were infected with lentivirus carrying MyD88 gene or shRNA to MyD88. MyD88 mRNA and protein expression was measured by RT-qPCR, immunohistochemistry and western blotting after infection for confirmation. Cell prolife-ration was detected by the WST-1 assay. Flow cytometry was used to measure the cell cycle and apoptosis. The transwell migration assay was used to observe the change of migration of transfected cells. The results showed that the overexpression of MyD88 increased the resistance of lung cancer A549 cells to paclitaxel, while the suppression of MyD88 increased the sensitivity of A549 lung cancer cells to paclitaxel. Following the paclitaxel treatment, a decreased apoptosis and G2 phase ratio, an increased cell migration ratio, and an increased production of IL-8 were found in MyD88‑overexpressed A549 cells. The western blot analysis revealed that Myd88 overexpression resulted in an increased level of Bcl-2 but a decreased level of Bax in A549 cells. These findings suggested that the expression level of MyD88 is closely associated with paclitaxel resistance in A549 lung cancer cells. Thus, the downregulation of MyD88 in A549 cells increased its sensitivity to paclitaxel treatment, whereas the upregulation of MyD88 substantiates its paclitaxel resistance.
authors.affiliation: Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Fenfen
authors.initials: F
authors.lastname: Xiang
authors.affiliation: Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Rong
authors.initials: R
authors.lastname: Wu
authors.affiliation: Central Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Zhenhua
authors.initials: Z
authors.lastname: Ni
authors.affiliation: Department of Ultrasound, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Chunying
authors.initials: C
authors.lastname: Pan
authors.affiliation: Central Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Yueping
authors.initials: Y
authors.lastname: Zhan
authors.affiliation: Central Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.affiliation: Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Xianpeng
authors.initials: X
authors.lastname: Meng
authors.affiliation: Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
authors.forename: Xiangdong
authors.initials: X
authors.lastname: Kang
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D017209:Apoptosis; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D019008:Drug Resistance, Neoplasm; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics* / Q000378:metabolism*; D017239:Paclitaxel / Q000494:pharmacology
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; D017239:Paclitaxel