BackgroundBreast cancer is the most common malignancy in women and the underlying mechanism of breast cancer cell metastasis is still far from uncover. Integrin subunit alpha 7 (ITGA7) is a functioning protein. It has been detected in many malignancies. But the function of ITGA7 in breast cancer is not clear. Our aim is to explore ITGA7 expression and its role in breast cancer.MethodsReal-time PCR was performed to determine ITGA7 expression in BC tissues and normal adjacent tissues. The specific functions of ITGA7 in breast cancer cell lines (MDA-MB-231 and BT-549) transfected with small interfering RNA were determined through migration, invasion assays. Western blot assays were performed to determine the expression of c-met and vimentin.ResultsITGA7 was down-regulated in breast cancer tissues compared to the adjacent normal tissues (T:N =7.68±27.38: 41.01± 31.47, P<0.001) and this observation was consistent with the TCGA cohort (T:N =4.51±0.45:5.40±0.61, P<0.0001). In vitro experiments showed that knocking down ITGA7 significantly inhibited the migration and invasion of the breast cancer cell lines (MDA-MB-231 and BT-549). Meanwhile, knockdown of ITGA7 promoted c-met and vimentin expression, which may induce invasion and migration.ConclusionITGA7 plays an important tumorigenic function and acts as a suppress gene in breast cancer. Our findings indicate that ITGA7 was the gene associated with breast cancer.
For women, breast cancer is the most commonly diagnosed cancer and the leading cause of women deaths due to cancer. In recent years, increasing long noncoding RNA (lncRNA) has been discovered to be related to tumorigenesis, progression, and prognosis. FOXD3-AS1 is a lncRNA and has been identified as a cancer-promoting gene in glioma. By analysing the FOXD3-AS1 expression in The Cancer Genome Atlas (TCGA) database, we found that FOXD3-AS1 has significantly high expression in breast cancer tumour comparing with the normal tissue. And patients with low FOXD3-AS1 expression had greater survival probability, smaller tumour size, and less distant metastasis. This leads us to peep inquisitively biological function of FOXD3-AS1 in breast cancer. Biological assays demonstrated that silenced FOXD3-AS1 impaired cell proliferation and inhibited cell migration and invasion in breast cancer cell lines (BT549, MDA-MB-231). These results suggest that FOXD3-AS1 could play a potential diagnostics or prognostic biomarker for patients with breast cancer. Significance of the study: We demonstrated that lncRNA FOXD3-AS1 has significantly high expression in breast cancer cell lines comparing with the normal tissue. Besides, our findings suggested that lncRNA FOXD3-AS1 could play a potential diagnostics or prognostic biomarker for patients with breast cancer. KEYWORDS FOXD3-AS1, breast cancer, invasion, lncRNA, migration 1 | INTRODUCTION Breast cancer is the first cause of new cancer diagnoses in women, approximately 30% of all new cases. And breast cancer is the second cause of leading cancer deaths; about 14% of all cancer deaths in women, the first cause is lung and bronchus cancer. From 2005 to 2014, breast cancer incidence has a slight increase. Nonwhite women promote the overwhelming majority of the increase (increases 1.7%per year among Asian and 0.3%-0.4% per year among Hispanic and black). 1,2 The higher diagnosing rate is probably because of the development of medical services and perfection of medical insurance. As the development of medical technology, significant advances have been made in the management of breast cancer. 3,4 But the death rate of breast cancer is still high, and patient outcomes still merit attention.As is known, tumorigenesis is related to the environment, living habits, aging, and so on. 5,6 But the molecular mechanisms of breast tumorigenesis still remain unclear. A lot of studies have discovered many oncogenes and tumour suppressor genes, which are acknowledged to be related to the occurrence of breast cancer. [7][8][9] Long noncoding RNAs as a heterogeneous class of noncoding RNAs, which are longer than 200 nucleotides, have been identified to involve in many human diseases, including tumorigenesis. 10,11 A few long noncoding RNAs (lncRNAs) have been identified as oncogenic or suppressor genes and regulate the progress of breast cancer. 12 lncRNA Yaoyao Guan and Adheesh Bhandari equally contributed to this study.
The incidence of thyroid cancer is staying at a high level. Claudin family is a skelemin contacting with the intercellular junction and can keep a dynamic balance between cells. Recently, many types of research indicated that the expression level of claudins is closely related to various cancer types and they can be novel diagnostic markers. For instance, Claudin-10(CLDN10) is the high expression in primary hepatocellular carcinoma, papillary thyroid cancer (PTC) and so on. But the biological role and function of CLDN10 in PTC are unclear. In our study, we measured the expression of CLDN10 in human normal tissues and matched PTC tissues by quantitative real-time polymerase chain reaction (qRT-PCR) and this observation was consistent with that in the TCGA cohort. We discovered that high expression of CLDN10 was correlated with lymph node metastasis, age and Histological type in TCGA cohorts. Kaplan-Meier analysis showed that patients with higher CLDN10 expression had a worse overall survival. In vitro, CLDN10 could promote cellular proliferation, migration, and invasion in PTC cell lines. In a word, CLDN10 is a functionally gene facilitating tumorgenesis in PTC and acts as an oncogene in PTC.
Thyroid cancer incidence has been continuity increasing worldwide. Uridine phosphorylase 1 (UPP1) is a protein‐coding gene and has been detected that UPP1 was the higher expression in many solid malignancies, just as head and neck cancers, breast cancer, compared with paired normal tissue. But the act of UPP1 in thyroid cancer is not explicit. In this article, we investigate the function of UPP1 expression in thyroid cancer. The Cancer Genome Atlas (TCGA) unpaired thyroid cancer and normal RNA‐seq data were downloaded, and our paired thyroid cancer and normal samples were analysed by a polymerase chain reaction. The expression of UPP1 was regulated by transfected small interfering RNA, and the function of UPP1 was determined via migration, invasion and cell proliferation assays. Western blot assay was achieved to determine the UPP1 expression correlates with the function of 5‐FU regulate epithelial‐mesenchymal transition. The significant upregulation of UPP1 in thyroid cancer tissues compared with normal thyroid tissues was revealed by our data and TCGA data. UPP1 overexpression was significantly correlated with lymph node metastasis, tumour stage and tumour size. In the cell, experiments showed that UPP1 low expression significantly suppressed the migration, invasion and proliferation. Western blot assay proves the effect of UPP1 expression on 5‐FU regulates epithelial‐mesenchymal transition pathway. UPP1 plays a crucial oncogene in thyroid cancer. Our findings indicate that UPP1 might be a biomarker of thyroid cancer and may act by regulating epithelial‐mesenchymal transition (EMT).
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