Open Access

ARTICLE

Knockdown Wiskott-Aldrich syndrome protein family member 3 (WASF3) inhibits colorectal cancer metastasis and sensitizes to cisplatin through targeting ZNF471

ZHIYONG ZHANG^1,#, YAN PAN^2,#, YAN ZHAO¹, MUDAN REN¹, YARUI LI¹, YUN FENG¹, GUIFANG LU^1,*, SHUIXIANG HE^1,*

1 Gastroenterology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710032, China
2 Cancer Biology, National Clinical Research Center for Digestive Diseases, and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi’an, 710032, China

* Corresponding Authors: Shuixiang He, ; Guifang Lu,
# These authors contributed equally to this work

BIOCELL 2022, 46(8), 1917-1924. https://doi.org/10.32604/biocell.2022.018847

Received 20 August 2021; Accepted 05 November 2021; Issue published 22 April 2022

Abstract

Colorectal cancer (CRC) is a heterogeneous cancer, and many risk factors for colorectal cancer have been established. For CRC metastasis, tumor cell migration, adhesion as well as invasion are important processes. WiskottAldrich syndrome protein family member 3 (WASF3) is necessary for metastasis of various types of cancers. However, its role in CRC progression has not been fully elucidated. This study examined the in vitro functional roles of WASF3 in the CRC and explored the underlying molecular mechanisms. We used siRNA-WASF3 to gene silence WASF3 in colon cancer cell (HCT116) in vitro. The effects of WASF3 silencing on HCT116 cell apoptosis, proliferation, migration, as well as invasion were assessed by flow cytometry, CCK-8, and transwell assays. ZNF471 protein expressions were detected by immunofluorescence staining and RT-PCR. Moreover, the effects of ZNF471 were studied on a series of in vitro antitumor-promoting assays using HCT116. WASF3 knockdown expression using small interfering RNA (siRNA) ameliorated CRC cell proliferation, anchorage-independent growth, invasion, and metastasis. Furthermore, we observed that WASF3 contributed to upregulating the metastasis signaling pathway through inhibiting the expression of ZNF471. Our study suggests that targeting WASF3 signaling might be a novel therapeutic strategy for treating CRC.

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