Background: Breast 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. Methods: Real-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. Results: ITGA7 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. Conclusion: ITGA7 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.

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).

The incidence of thyroid cancer has increased in the past decades; however, the underlying molecular mechanisms of thyroid cancer tumorigenesis remain unknown. Using sequencing technology, long intergenic non‑protein coding RNA 673 (LINC00673) was identified to be upregulated in several tumor tissues. However, the biological role of LINC00673 in thyroid carcinoma has yet to be determined. In this study, 60 matched pairs of thyroid tumor tissue and normal tissue were selected for study using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to validate previous findings; then, clinicopathologic features of the tissues were analyzed. Proliferation, colony formation, migration and invasion assays were performed, and epithelial-mesenchymal transition (EMT)-associated phenotypes were investigated following transfection with small interfering RNA to determine the specific role of LINC00673 in thyroid carcinoma cell lines (TPC1, KTC‑1 and BCPAP). The study revealed that long non‑coding RNA LINC00673 was significantly upregulated in thyroid cancer tissues compared with paired adjacent non‑tumor tissues using RT-qPCR and that high expression of LINC00673 is was associated with larger tumor size and lymph node metastasis in the validated cohort. Knockdown of LINC00673 inhibited cell proliferation and metastasis, whereas, LINC00673 overexpression had the opposite effect. The results showed that LINC00673 may influence EMT and the expression of Kruppel-like factor 2 (KLF2). Notably, KLF2 is considered a tumor suppressor gene in a variety of tumors. Finally, knock down of KLF2 enhanced thyroid carcinoma cell proliferation, and invasion and migration. In this study, the function of LINC00673 in promoting the proliferation and metastasis of thyroid carcinoma cell lines was identified, and LINC00673 may act as a novel therapeutic target for treating thyroid carcinoma.