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<p>To explore the regulatory effect of c-Jun N-terminal kinase (JNK) inhibitor (SP600125) on forkhead box protein L2 (FOXL2) gene in human ovarian granulosa cell tumor cells (KGN cells). The main pathogenic gene FOXL2 of ovarian cancer was screened by bioinformatics method. KGN cells were randomly divided into control group and experimental group. Different concentrations of SP600125 (0.1, 1, 5, 10, 50 µM) were added to the experimental group, and an equal volume of dimethyl sulfoxide (DMSO) was added to the control group. The cells were incubated for 48&#xa0;h. Cell RNA was extracted and reverse transcribed into cDNA. The mRNA expression level of FOXL2 was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Proteins were extracted, and the expression level of FOXL2 protein was detected by Western blot. The proliferation ability of KGN cells treated with SP600125 was detected by MTT assay. Cell scratch assay was used to detect its migration ability. Different concentrations of JNK inhibitor reduced the expression of FOXL2 in ovarian granulosa cells KGN, and 1 µM had the best inhibitory effect. JNK inhibitor reduces the expression of FOXL2 in ovarian granulosa cell tumor KGN.</p>

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Regulation of FOXL2 gene in ovarian granulosa cell tumor by JNK inhibitor

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月9日

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  • Yuzhu Zhang,
  • Yu Wang,
  • Yuan Gu,
  • Yang Liu,
  • Guohua Liu,
  • Jun Wu,
  • Nan Bai

摘要

To explore the regulatory effect of c-Jun N-terminal kinase (JNK) inhibitor (SP600125) on forkhead box protein L2 (FOXL2) gene in human ovarian granulosa cell tumor cells (KGN cells). The main pathogenic gene FOXL2 of ovarian cancer was screened by bioinformatics method. KGN cells were randomly divided into control group and experimental group. Different concentrations of SP600125 (0.1, 1, 5, 10, 50 µM) were added to the experimental group, and an equal volume of dimethyl sulfoxide (DMSO) was added to the control group. The cells were incubated for 48 h. Cell RNA was extracted and reverse transcribed into cDNA. The mRNA expression level of FOXL2 was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Proteins were extracted, and the expression level of FOXL2 protein was detected by Western blot. The proliferation ability of KGN cells treated with SP600125 was detected by MTT assay. Cell scratch assay was used to detect its migration ability. Different concentrations of JNK inhibitor reduced the expression of FOXL2 in ovarian granulosa cells KGN, and 1 µM had the best inhibitory effect. JNK inhibitor reduces the expression of FOXL2 in ovarian granulosa cell tumor KGN.