Corylin, a biologically active agent extracted from Psoralea corylifolia L. (Fabaceae), promotes bone differentiation and inhibits
inflammation. Currently, few reports have addressed the
biological functions that are regulated by
corylin, and to date, no studies have investigated its antitumor activity. In this study, we used cell functional assays to analyze the antitumor activity of
corylin in
hepatocellular carcinoma (HCC). Furthermore, whole-transcriptome assays were performed to identify the downstream genes that were regulated by
corylin, and gain-of-function and loss-of-function experiments were conducted to examine the regulatory roles of the above genes. We found that
corylin significantly inhibited the proliferation, migration, and invasion of HCC cells and increased the toxic effects of chemotherapeutic agents against HCC cells. These properties were due to the induction of a
long noncoding RNA, RAD51-AS1, which bound to RAD51
mRNA, thereby inhibiting
RAD51 protein expression, thus inhibiting the DNA damage repair ability of HCC cells. Animal experiments also showed that a combination treatment with
corylin significantly increased the inhibitory effects of the chemotherapeutic agent
etoposide (
VP16) on
tumor growth. These findings indicate that
corylin has strong potential as an adjuvant
drug in HCC treatment and that
corylin can strengthen the therapeutic efficacy of
chemotherapy and
radiotherapy.