Integrin α7 high expression correlates with deteriorative tumor features and worse overall survival, and its knockdown inhibits cell proliferation and invasion but increases apoptosis in breast cancer

Abstract

Background This study aimed to investigate the correlation of integrin α7 (ITGA7) expression with clinical/pathological characteristics and overall survival (OS), and its knockdown on inhibiting cell activities in breast cancer. Methods A total of 191 breast cancer patients underwent surgery were retrospectively reviewed, and ITGA7 expression in tumor tissues was determined by immunofluorescence and real‐time quantitative polymerase chain reaction. Patients’ clinical/pathological data were recorded, and OS was calculated. In vitro, control shRNA and ITGA7 shRNA plasmids were transfected into MCF7 cells to evaluate the influence of ITGA7 knockdown on cell proliferation, apoptosis, and invasion. Results Ninety‐two (48.2%) patients presented with ITGA7 high expression, and 99 patients (51.8%) presented with ITGA7 low expression. ITGA7 expression was positively correlated with T stage, tumor‐node metastasis (TNM) stage, and pathological grade. Kaplan‐Meier curves showed that ITGA7 high expression was associated with shorter OS, and multivariate Cox's proportional hazards regression displayed that ITGA7 high expression was an independent predictive factor for poor OS. Moreover, in vitro experiments disclosed that cell proliferation (by Cell Counting Kit‐8 assay) and cell invasion (by Matrigel invasion assay) were reduced, while cell apoptosis rate (by Annexin V/propidium iodide assay) was enhanced by ITGA7 knockdown in MCF‐7 cells. Conclusion Integrin α7 high expression correlates with increased T stage, TNM stage, and pathological grade as well as worse OS, and its knockdown enhances cell apoptosis but inhibits cell proliferation and invasion in breast cancer.

Predictive value of integrin α7 for acute myeloid leukemia risk and its correlation with prognosis in acute myeloid leukemia patients

“…Another recent report provides strong in vitro and in vivo evidence that ITGA7 interacts with laminin‐induced outside‐in signaling to participant in the growth and invasion of glioblastoma stem‐like cells . Meanwhile, an interesting in vitro experiment reveals that ITGA7 knockdown reduces cell proliferation and cell invasion, while enhances cell apoptosis rate in breast cancer cells . Additionally, a previous study highlights a surprising function of ITGA7 as a tumor promoter in OSCC malignancy that ITGA7 not only upregulates stemness‐associated genes expressions (such as octamer‐binding transcription factor 4 [OCT4], SRY [sex‐determining region Y]‐box 2 [SOX2], Nanog homeobox [NANOG] and CD90), but also enhances abilities to self‐renew of OSCC cells via activating the FAK‐mediated signaling pathways .…”

Integrin α7 knockdown suppresses cell proliferation, migration, invasion and EMT in hepatocellular carcinoma

“…Previous studies indicated that ITGA7 is involved in the pathological progression of different carcinomas through affecting cell activities such as cell migration and invasion (5,6,9,(13)(14)(15). For example, the interaction between ITGA7 and laminin-induced outside-in signaling contributed to glioblastoma stem-like cell growth and invasion (12).…”

“…In another study, ITGA7 promoted the stemness of OSCC cells via FAK/MAPK/ERK signaling, which subsequently induced the tumorigenicity and metastasis of OSCC (5). In addition, ITGB7 knockdown enhanced cell apoptosis but inhibited cell proliferation and invasion in breast cancer (14). Although a few studies have been performed to explore the role of ITGA7 in different types of carcinoma, there remain certain contradictions.…”

Tumor Nonimmune-Microenvironment-Related Gene Expression Signature Predicts Brain Metastasis in Lung Adenocarcinoma Patients after Surgery: A Machine Learning Approach Using Gene Expression Profiling

“…A high expression of COL5A2 is associated with metastasis in renal cell carcinoma [88]. ITGA7 upregulation promotes the proliferation and invasion of breast cancer cells [89].…”