ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

Abstract

BackgroundPrevious research found that ALG3 is associated with cervical cancer, but the role of ALG3 in breast cancer was still unknown.Material/MethodsThe expression of ALG3 in breast carcinoma tissues was determined by immunochemistry. The ability of cellular proliferation, migration, and invasion was determined by CCK-8 assay, wound healing migration assay, and cell invasion assays, respectively. The binding between HSF2 and promoter of ALG3 was determined by ChIP assay.ResultsThere was an increased expression of ALG3 in breast cancer tissues compared to normal breast tissues (p<0.05). High expression of ALG3 was significantly correlated with poor OS (p<0.05). ALG3 expression was significantly increased in cancer samples with advanced stages (stage III/IV) compared with those in the early stages of disease (stage I/II) (p<0.05). The staining intensity of ALG3 was significantly correlated to the tumor grade (grades 2–3 versus 1, p<0.05). Silencing ALG3 or HSF2 inhibited the proliferation, migration, and invasion abilities of MCF-7 cells. Silencing ALG3 retarded the growth of MCF-7 cells in vivo.ConclusionsSilencing ALG3 inhibited MCF-7 cells growth in vitro and in vivo. HSF2 activated ALG3 and promoted the growth of breast carcinoma.

ALG3 Contributes to the Malignant Biological Properties of Oral&nbsp;Squamous&nbsp;Cell&nbsp;Carcinoma Cells Through Regulating CDK-Cyclin Pathway

“…According to previous studies, ALG3 has been reported to be an underlying treatment target in non-small cell lung cancer [15], and high expression of ALG3 was positively correlated with the rapid development and poor prognosis of breast cancer patients [10]. Similar to previous studies, our results discovered that ALG3 was highly expressed in OSCC tissues and cell lines.…”

“…By analyzing the TCGA database including 338 OSCC tumor and 32 normal tissues, ALG3 was picked up for further exploration. The data from TCGA presented that ALG3 was obviously enhanced in OSCC tumor tissues, which was consisted with the expression in esophageal squamous cell carcinoma and breast cancer [8,10] (Fig. 1A, p=4.735e-03).…”

Novel variants and clinical symptoms in four new ALG3‐CDG patients, review of the literature, and identification of AAGRP‐ALG3 as a novel ALG3 variant with alanine and glycine‐rich N‐terminus

“…Recently and in line with this, ALG3 was also detected in cellular compartments apart from the ER, albeit the function of this protein in the cytosol and nucleus remains unclear (Hacker, Schultheiss, & Kurzik‐Dumke, ; Hacker, Schultheiss, Doring, & Kurzik‐Dumke, ). Furthermore, ALG3 seems to be associated with cervical cancer (Yang et al, ) and was also found to affect drug‐resistance in acute myeloid leukemia cells (Liu et al, ).…”

HSF2 is a Promising Prognostic Biomarker and is Correlated With Immune Infiltration in Hepatocellular Carcinoma

“…The miR-183/-96/-182 cluster then promotes the migration and survival of breast cancer cells by inhibiting the expression of the tumor suppressor RAB21 [36]. In breast cancer cells, HSF2 can regulate ALG3 enzyme expression to enhance cell proliferation and migration [37]. Moreover, knockdown of ALG3 reduces tumor growth and HSF2 expression levels, indicating feedback between HSF2 and ALG3 [37].…”

“…In breast cancer cells, HSF2 can regulate ALG3 enzyme expression to enhance cell proliferation and migration [37]. Moreover, knockdown of ALG3 reduces tumor growth and HSF2 expression levels, indicating feedback between HSF2 and ALG3 [37]. Moreover, miR-202 is aberrantly expressed in ESCC and negatively regulates apoptosis by directly targeting HSF2 and subsequently affecting HSP70 expression [25].…”