Numerous evidence has recently demonstrated that long non-coding RNAs (lncRNAs) play vital roles in the oncogenesis and development of a wide range of human neoplasms. Leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1), a novel cancer-related lncRNA, has been reported to be under-expressed in breast cancer and associated with poor prognosis. However, the exact role of LIFR-AS1 in breast cancer remains largely unclear. The present study aimed to investigate the biological role of LIFR-AS1 in breast cancer and clarify the potential molecular mechanisms. In the present study, we found that LIFR-AS1 was significantly down-regulated in both tissues and cell lines. Furthermore, over-expression of LIFR-AS1 inhibited breast cancer cell proliferation, colony formation, migration and invasion, whereas knockdown of LIFR-AS1 promoted breast cancer cell proliferation, colony formation, migration and invasion. Moreover, LIFR-AS1 was observed to up-regulate suppressor of fused gene (Sufu) expression by competitively binding to miR-197-3p in breast cancer cells. Notably, miR-197-3p inhibitor reversed the promoting effects of LIFR-AS1 knockdown on breast cancer cell proliferation, colony formation, migration and invasion. Additionally, LIFR-AS1 knockdown promoted tumor growth in vivo. To sum up, our results imply the tumor-suppressing role of LIFR-AS1 in breast cancer.

Purpose The aim of this study was to research the effect of miR‐202 on breast cancer cells proliferation, invasion, and migration. Methods TCGA analysis was used to research miR‐202 expression and overall survival in patients with breast cancer. Transfection with miR‐202 mimics or cotransfection with miR‐202 mimics and ROCK1 expression vector was performed on breast cancer cells. Reverse transcription polymerase chain reaction was used to detect the miR‐202 expression of breast cancer tissues and cells. Western blot was conducted to research the expression of ROCK1, E‐cadherin, Twist, N‐cadherin, and MMP2. Dual luciferase reporter assay was performed to detect the targeted relationship between ROCK1 and miR‐202. MTT and transwell assay were used to detect breast cancer cells proliferation, invasion, and migration. Results Downregulation of miR‐202 was positively correlated with poor prognosis of patients with breast cancer. miR‐202 in breast cancer tissues and breast cancer cells was significantly downregulated. Upregulation of miR‐202 inhibited the proliferation, migration, and invasion of breast cancer cells. miR‐202 promoted E‐cadherin expression and inhibited the expression of N‐cadherin, Twist, and MMP2. ROCK1 was the target gene of miR‐202. miR‐202 regulated proliferation, migration, invasion, and expression of related proteins in breast cancer cells by targeting ROCK1 expression. Conclusions miR‐202 inhibited breast cancer cells proliferation, invasion, and migration by targeting the ROCK1 gene

Background Gastric cancer (GC) is one of the most common digestive system diseases and yet lacks effective therapeutic regimen. Aims The aim of our present research was to probe the value of hsa_circ_0001017 in GC treatment. Methods qRT-PCR and Western blot were performed to detect gene and protein expressions, respectively. CCK-8 assay and clone formation assay were used to ensure the proliferation of GC cell lines. Transwell assay was performed to measure the migration and invasion of GC cell lines. The relationship between hsa_circ_0001017 and miR-197 and that between miR-197 and RHOB 3′-UTR were ensured using the luciferase reporter assay. Results Decreased hsa_circ_0001017 was discovered in GC, and upregulation of hsa_circ_0001017 notably repressed proliferation, migration, and invasion of GC cell lines. We further certificated that hsa_circ_0001017 served as miR-197 sponge and suppressed the expression of miR-197. Moreover, hsa_circ_0001017 upregulation meaningfully accelerated RHOB expression in both gene and protein levels, and RHOB was a downstream target of miR-197. Overexpression of miR-197 could markedly restrain hsa_circ_0001017-induced RHOB increasing and stifle inhibition of hsa_circ_0001017 to the malignant phenotype of GC cell lines. Next, our results further confirmed that hsa_circ_0001017 increasing notably inhibited tumor growth, impeded miR-197 production, while it enhanced the expression of RHOB in vivo. Conclusion Our data demonstrated that upregulation of hsa_circ_0001017 could notably muffle the proliferation as well as the metastasis of GC cell lines and impede the formation of GC tumor via targeting to miR-197/RHOB signaling pathway. Our results evidenced that hsa_circ_0001017 may act as a rising biomarker for GC treatment.

Polyphenolic compounds present in fruits, vegetables and grains are bioactive molecules which elicit a wide range of responses both in vivo and in vitro. The aim of this study is to investigate whether the soybean isoflavone, equol could induce apoptosis in ovarian cancer cells, SKOV-3. In this study, we evaluated molecular events associated with apoptosis induced by equol and paclitaxel (PTX). To assess whether growth inhibition was due to apoptosis, flow cytometry, colorimetry experiments, immunoblot analyses through measuring DNA fragmentation, the level of TRAIL, the cleavage of poly(ADP-ribose) polymerase (PARP) and the activation of caspase-3, -8 and -9 were also performed. Results showed that apoptosis was induced by extrinsic pathway triggered by TNF family members. Overall results suggested that equol induces apoptosis in SKOV-3 cells via a TRAIL and caspase 8-dependent pathway whereas paclitaxel leads to smaller apoptotic events when compared to that of equol.