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Anillin actin binding protein (ANLN) is involved in various human cancers. It is often upregulated in various cancers, including cervicalcancer (CC). However, the exact role of ANLN in the modulation of CC andthe underlying molecular mechanism remain unknown. In this study, weaimed to investigate the effects of ANLN on the proliferation, migration,and invasion of CC cells, as well as to determine the molecular mechanismsunderlying these effects.    Material and methods  ANLN expression levels were analyzed in normalcervical and CC specimens using public databases and tissue samples. Theprognosis was determined using the TCGA database. Cell proliferation, migration and invasion were measured by Edu assay, wound-healing assay andtranswell assay, respectively. Immunofluorescence was used to examine theinfluence of ANLN inhibition on actin stress fiber integrity. Western blotswere used to measure the protein expression.    Results  ANLN expression levels in CC were higher than those in normal tissues, and ANLN overexpression was highly correlated with poor prognosis.ANLN knockdown inhibited CC cell proliferation, migration, and invasion invitro, while ANLN overexpression led to an inverse biological phenotype. Immunofluorescence showed that ANLN inhibition could influence actin stressfiber integrity. ANLN expression was positively correlated with ROCK1 andROCK2 expression in CC. Overexpression of ANLN activated RhoA and upregulated ROCK1 and ROCK2. Furthermore, ROCK1 and ROCK2 expression levelswere also impeded by Y27632, which is a specific inhibitor of RhoA. Theyalso weakened the migration and invasion ability in ANLN-overexpressionHeLa cells.    Conclusions  ANLN promotes cell migration and invasion through RhoAROCK signaling in CC.

ANLN promotes cell migration and invasion through RhoA-ROCK signaling in cervical cancer