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Fig. 5 | Journal of Hematology & Oncology

Fig. 5

From: Overexpression of CLC-3 is regulated by XRCC5 and is a poor prognostic biomarker for gastric cancer

Fig. 5

The expression of CLC-3 was regulated at the transcriptional level by XRCC5 interacting with PARP1. a The binding of XRCC5 to the CLC-3 DNA in SGC-7901 cells was suppressed after XRCC5 knockdown. b Knockdown of XRCC5 impaired the promoter activities of the pGL4.10-CLC-3 − 248 and pGL4.10-CLC-3 − 538 reporter plasmids in SGC-7901 cells (n = 3). c The RNA level of CLC-3 was reduced after XRCC5 knockdown and increased after XRCC5 overexpression (n = 3). d Knockdown of XRCC5 decreased the levels of key targets in the PI3K/Akt signaling pathway by downregulating CLC-3 in SGC-7901 cells. e–g PARP1 was identified as an interaction partner of XRCC5 by IP and MS in nuclear protein extracts of SGC-7901 cells. h The interaction between XRCC5 and PARP1 was confirmed by Co-IP in stable SGC-7901 cells with XRCC5 overexpression. i Binding between PARP1 and the CLC-3 promoter was detected by WB in the nuclear protein/DNA complex using synthesized probe or NSP. j The co-localization of XRCC5 and PARP1 was observed in the nucleus by confocal microscopy analysis. k Overexpression of XRCC5 increased the expression of CLC-3 in SGC-7901 cells, and the increase effect could be reversed by the PARP1 knockdown. l, m The proliferation and clonogenicity of SGC-7901 cells were promoted by XRCC5 overexpression, and the promotion effects were reversed by PARP1 knockdown (n = 3). *P < 0.05, **P < 0.01

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