Department of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China.
Department of Cell Biology, School of Life Sciences, China Medical University, Shenyang, China.
Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820980074. doi: 10.1177/1533033820980074.
We aimed to identify the expression of Sal-like 4 (SALL4) in breast cancer tissues and to explore the role of this gene in the carcinogenesis of breast cancer cells.
A total of 62 paired breast cancer and noncancerous tissue samples were obtained from patients with breast cancer. SALL4 expression patterns and their association with clinicopathological characteristics were investigated by qRT-PCR, western blotting, and immunochemistry in breast cancer tissues. After the knockdown of SALL4 by short hairpin RNAs (shRNAs), the proliferative, invasive, and apoptotic abilities of MDA-MB-435 and MDA-MB-468 cells (breast cancer cell lines) were measured by colony formation and CCK-8 assays, wound healing and transwell assays, and flow cytometry, respectively.
SALL4 expression was higher in breast cancer tissues than that in the paired noncancerous tissues, and increased SALL4 expression in tumor tissues was closely related to tumor size and lymphatic metastasis. Furthermore, functional experiments revealed that SALL4 knockdown inhibited the cell proliferation, induced cell cycle arrest in G0/G1phase and apoptosis, and decreased the ability of migration and invasion in breast cancer cells. Additionally, our study first demonstrated that SALL4 played a critical role in modulating the tumorigenicity of breast cancer cells via the WNT/β-catenin signaling pathway.
Our results suggest that the expression of SALL4 is upregulated in breast cancer, and this upregulation is involved in the regulation of cell growth, invasion, and apoptosis. Hence, SALL4 may be a promising target for diagnosis and therapy in patients with breast cancer.
我们旨在鉴定 Sall 样 4（SALL4）在乳腺癌组织中的表达，并探讨该基因在乳腺癌细胞发生中的作用。
收集 62 对乳腺癌及癌旁组织标本，采用 qRT-PCR、western blot 和免疫组化检测 SALL4 在乳腺癌组织中的表达模式及其与临床病理特征的关系。通过短发夹 RNA（shRNA）敲低 SALL4 后，通过集落形成和 CCK-8 测定、划痕愈合和 Transwell 测定以及流式细胞术分别测定 MDA-MB-435 和 MDA-MB-468 细胞（乳腺癌细胞系）的增殖、侵袭和凋亡能力。
与配对的非癌组织相比，SALL4 在乳腺癌组织中的表达水平更高，且肿瘤组织中 SALL4 的高表达与肿瘤大小和淋巴转移密切相关。此外，功能实验表明，SALL4 敲低抑制了乳腺癌细胞的增殖，诱导 G0/G1 期细胞周期停滞和凋亡，并降低了迁移和侵袭能力。此外，我们的研究首次表明，SALL4 通过 WNT/β-catenin 信号通路在调节乳腺癌细胞的致瘤性方面发挥着关键作用。
我们的研究结果表明，SALL4 在乳腺癌中表达上调，这种上调参与了细胞生长、侵袭和凋亡的调节。因此，SALL4 可能是乳腺癌患者诊断和治疗的一个有前途的靶点。
