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Transcription Factor CTCFL Promotes cell Proliferation, Migration and Invasion in Gastric Cancer Via Activating DPPA2

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Abstract Background: The purpose of this study was to explore the relationship between CTCFL and DPPA2, and validate the positive role of CTCFL/DPPA2 in cell proliferation, migration and invasion in gastric cancer.Methods: Bioinformatics methods were applied for the prediction of gastric cancer-related transcription factors and corresponding target mRNAs. qRT-PCR and western blot were performed to test the levels of CTCFL and DPPA2. Then a series of in vitro experiments were conducted to assay the cell biological behaviors, including CCK-8, colony formation assay, wound healing assay and Transwell invasion assay. CHIP was carried out for assessment of the targeted relationship between CTCFL and DPPA2.Results: CTCFL and DPPA2 were both highly expressed in gastric cancer cells, and high CTCFLL and DPPA2 could promote cell proliferation, migration and invasion. CHIP validated that DPPA2 was a target of CTCFL. In addition, high DPPA2 could reverse the inhibitory effect of CTCFL silencing on the cell proliferation, migration and invasion in gastric cancer.Conclusion: The transcription factor CTCFL promotes cell proliferation, migration and invasion in gastric cancer via activating DPPA2.
Springer Science and Business Media LLC
Title: Transcription Factor CTCFL Promotes cell Proliferation, Migration and Invasion in Gastric Cancer Via Activating DPPA2
Description:
Abstract Background: The purpose of this study was to explore the relationship between CTCFL and DPPA2, and validate the positive role of CTCFL/DPPA2 in cell proliferation, migration and invasion in gastric cancer.
Methods: Bioinformatics methods were applied for the prediction of gastric cancer-related transcription factors and corresponding target mRNAs.
qRT-PCR and western blot were performed to test the levels of CTCFL and DPPA2.
Then a series of in vitro experiments were conducted to assay the cell biological behaviors, including CCK-8, colony formation assay, wound healing assay and Transwell invasion assay.
CHIP was carried out for assessment of the targeted relationship between CTCFL and DPPA2.
Results: CTCFL and DPPA2 were both highly expressed in gastric cancer cells, and high CTCFLL and DPPA2 could promote cell proliferation, migration and invasion.
CHIP validated that DPPA2 was a target of CTCFL.
In addition, high DPPA2 could reverse the inhibitory effect of CTCFL silencing on the cell proliferation, migration and invasion in gastric cancer.
Conclusion: The transcription factor CTCFL promotes cell proliferation, migration and invasion in gastric cancer via activating DPPA2.

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