Background Breast cancer is the most common malignant tumor that threatens women's health. The study of long-chain non-coding RNA (lncRNA) in breast cancer has been paid more and more attention, which is related to the progression of breast cancer, but the specific mechanism is not clear. Methods In this study, we explored the role of lncRNA BC069792 in breast cancer. In vitro and in vivo functional experiments were carried out in cell culture and mouse models. High-throughput next-generation sequencing technology and real-time fluorescence quantitative PCR technology were used to evaluate differentially expressed genes and mRNA expression, Western blot and immunohistochemical staining were used to detect protein expression. RNA immunoprecipitation assay and dual-luciferase activity assay were used to evaluate the competing endogenous RNAs (ceRNA), and rescue and mutation experiments were used for verification. Results We found that lncRNA BC069792 was expressed at low level in breast cancer tissues, and significantly decreased in breast cancer with high pathological grade, lymph node metastasis and high Ki-67 index groups. Moreover, BC069792 inhibited the proliferation, invasion and metastasis of breast cancer cells in vitro and in vivo. Mechanically, BC069792 acts as a molecular sponge to adsorb hsa-miR-658 and hsa-miR-4739, to up-regulate the protein expression of Potassium Voltage-Gated Channel Q4 (KCNQ4), inhibit the activities of JAK2 and p-AKT, and play a role in inhibiting breast cancer growth. Conclusions LncRNA BC069792 plays the role of tumor suppressor gene in breast cancer and is a new diagnostic index and therapeutic target in breast cancer.

Long non-coding RNAs (LncRNAs) have already been taken as critical regulatory molecules in breast carcinoma (BC). Besides, the progression of BC is closely associated with the immune system. However, the relationship between lncRNAs and the tumor immune system in BC has not been fully studied. LncRNA KRT19P3 has been reported to inhibit the progression of gastric cancer. In the present study, we first discovered that KRT19P3 was downregulated in BC tissues compared with para cancer tissue. Then we showed that KRT19P3 could be used as a marker to differentiate BC from para cancer tissue. Increased expression of KRT19P3 markedly inhibited the proliferation, migration, and invasion rate of BC cells in vitro and tumor growth of BC in vivo. Conversely, KRT19P3 knockdown by siRNA markedly promoted the proliferation, migration, and invasion rate of BC cells after being transfected. Comparison of clinical parameters showed an inverse relationship between the expression of KRT19P3 and pathological grade. Furthermore, immunohistochemistry (IHC) was applied to reveal the positive rate of the expression of Ki-67, programmed death-ligand 1 (PD-L1), and CD8 in BC tissues. Correlation analysis showed that Ki-67 and PD-L1 were inversely proportional to KRT19P3 but CD8 was directly proportional to KRT19P3. In conclusion, this study demonstrated that lncRNA KRT19P3 inhibits BC progression, and may affect the expression of PD-L1 in BC, which in turn affects CD8+ T (CD8 positive Cytotoxic T lymphocyte) cells in the immune microenvironment.

In recent years, the role of potassium channels in tumors has been intensively studied. Potassium channel proteins are widely involved in various physiological and pathological processes of cells. The expression and dysfunction of potassium channels are closely related to tumor progression. Potassium channel blockers or activators present antitumor effects by directly inhibiting tumor growth or enhancing the potency of classical antitumor agents in combination therapy. This article reviews the mechanisms by which potassium channels contribute to tumor development in various tumors in recent years, introduces the potential of potassium channels as diagnostic targets and therapeutic means for tumors, and provides further ideas for the proper individualized treatment of tumors.