MicroRNA­192 inhibits cell proliferation and induces apoptosis in human breast cancer by targeting caveolin 1.

It has been demonstrated that microRNA­192 (miR­192) serves important roles in different cancer types, including breast cancer, prostate cancer and colorectal cancer. However, its biological role and function in breast cancer remains largely unknown. The present study aimed to determine the role of miR­192 in breast cancer. In the present study, one normal breast and two breast tumor cells lines were used, which included the normal mammary fibroblast cell line Hs578Bst, a more aggressive breast tumor cell line MDA­MB­231 and a less aggressive breast tumor cell line MCF­7. The effect of miR­192 on proliferation of breast cancer cells was detected with an MTT assay. Western blot analysis was performed to determine protein expression of caveolin 1 (CAV1). A lentiviral vector that overexpresses pre­miR­192 and control lentiviral packaging plasmids were used in the present study. The Student's t­test was performed to analyze the significance of differences between samples. In the present study, it was determined that the expression of miR­192 is downregulated in breast cancer, compared with the adjacent normal tissues. Overexpression of miR­192 significantly inhibited cell proliferation, and induced cell apoptosis and cell cycle arrest in MCF7 and MDA­MB­231 cells. Using a bioinformatics method, CAV1 was considered a potential target of miR­192. Furthermore, it was demonstrated that CAV1 is a direct target of miR­192 and its protein expression is negatively regulated by miR­192. Therefore, the present study demonstrated that miR­192 serves an important role as a regulator in breast cancer and the miR­192/CAV1 axis has a potential as a therapeutic target for treatment of breast cancer.

Apatinib suppresses breast cancer cells proliferation and invasion via angiomotin inhibition.

Breast cancer is a leading cause of cancer-related death in the women worldwide. Apatinib is a novel tyrosine kinase inhibitor that selectively binds and inhibits vascular endothelial growth factor receptor 2 (VEGFR-2). The clinical trials have demonstrated the objective efficacy of Apatinib against metastatic breast cancer. However, the underlying mechanism is not well established. In the present study, the breast cell lines, BT-474 and MCF-7, were investigated. The effect of Apatinib on the cell viability was determined using CCK-8 assay. The migration, invasion, cell cycle distribution and the downstream signaling of VEGFR-2 in the cells were determined after 48 h treatment with this drug. Subsequently, Vector of angiomotin (AMOT) cDNA was transfected into MCF-7 cells. The cells were either exposed to Apatinib or vehicle and then examined for cell viabilities, migration, invasion, cell cycle distribution and the downstream signaling of VEGFR-2. Apatinib demonstrated a dose-dependent, significant inhibition of cell viabilities, migration and invasion of BT-474 and MCF-7 cells, with an increase in the percentage of cells in G1 phase and a decrease in S phase. In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1. The inhibitory effect of Apatinib on the cell activities and protein expressions were significantly suppressed by AMOT overexpression. The results of this study indicated that Apatinib inhibited MCF-7 cell proliferation and invasion through AMOT/VEGFR-2 pathway.

LncRNA NEF inhibits migration and invasion of HPV-negative cervical squamous cell carcinoma by inhibiting TGF-ß pathway.

LncRNA NEF was a recently identified tumor suppressor lncRNA in hepatocellular carcinoma. Our study aimed to explore the role of NEF in cervical squamous cell carcinoma (CSCC) patients. In the present study, expression of NEF in tumor tissue (cervical biopsies for healthy control) and serum of human papillomaviruses (HPV)-negative and HPV-positive CSCC patients as well as healthy controls was detected by qRT-PCR. Diagnostic and prognostic values of NEF for CSCC were evaluated by ROC curve and survival curve analysis, respectively. NEF expression vector was transfected into CSCC cells and the effects on cell migration and invasion as well as TGF-ß1 expression were investigated by Transwell migration assay, Transwell invasion assay, and Western blot, respectively. We found that expression of NEF in cervical tissues (tumor tissues for CSCC patients) and serum was significantly down-regulated in HPV-negative CSCC patients than in healthy controls and HPV positive patients, but no significant differences were found between healthy controls and HPV positive patients. Low serum levels of NEF distinguished HPV-negative CSCC patients from healthy controls and indicated poor survival. NEF overexpression inhibited the migration and invasion of HPV-negative but not HPV-positive CSCC cells. NEF overexpression down-regulated TGF-ß1 in HPV-negative CSCC cells but not in HPV-positive CSCC cells. TGF-ß1 treatment reduced the effects of NEF overexpression on cell migration and invasion. Therefore, we conclude that lncRNA NEF may inhibit the migration and invasion of HPV-negative cervical squamous cell carcinoma by inhibiting TGF-ß pathway.

Laparoscopic surgery is feasible for the treatment of rectal cancer after neoadjuvant chemoradiotherapy.

This case-control study aimed to clarify the short- and long-term outcomes of laparoscopic surgery for rectal cancer after neoadjuvant chemo radiotherapy compared with conventional open resection. Between January 2008 and December 2014, a series of 227 patients with rectal cancer underwent radical surgery after neoadjuvant chemo radiotherapy. Age, gender, American Society of Anesthesiologists score, clinical stage, and type of resection were matched by propensity scoring and 106 patients (53 patients with laparoscopic total mesorectal excision and 53 patients with open resection) were selected for analysis. There were no significant differences in the clinicopathological features between the two groups. With regard to short-term outcomes, blood loss, postoperative analgesia and hospital stay were significantly shorter in the laparoscopy group than in the open group, whereas operative time was significantly longer in the laparoscopy group than in the open group. The overall morbidity was similar in the two groups. There were no significant differences in the 5-year overall and disease-free survival rates between the two groups. In summary, laparoscopic surgery may be both feasible and efficient compared with open resection for rectal cancer after neoadjuvant chemo radiotherapy.

X-linked inhibitor of apoptosis-associated factor l (XAFl) enhances the sensitivity of colorectal cancer cells to cisplatin.

The purpose of present study was to investigate the roles of X-linked inhibitor of apoptosis-associated factor l (XAFl) in regulation apoptosis of colorectal cancer (CRC) cells after treatment with cisplatin (DDP). A total of ten paired cancerous and non-cancerous tissues were collected from patients with CRC after surgery. The levels of XAFl protein were detected by Western blot. Primary CRC cells were separated from cancer tissues, and its viability or apoptosis after treatment with DDP was determined with MTT or Annexin V/PI assays, respectively. Furthermore, we either up-regulated transfecting a XAF1 overexpression vector or down-regulated XAF1 by siRNA interference. And then, the XAF1 levels and its sensitivity to cisplatin were assessed. XAFl had a lower expression in the cancerous tissues from samples T1, T2 and T3 than their paired non-cancerous tissues N1, N2 and N3. However, the expression of XAF1 was not detected in samples T4 and N1. XAF1 levels in cancer tissues significantly decreased in comparison with normal tissues. Cell abilities of primary cells were significantly decreased in a dose-dependent manner, after treatment with a series concentrations of cisplatin (2, 5, 10 µg/mL) for 48 h. Although, after down-expression of XAFl by siRNA, cisplatin caused a significant decreases in apoptosis rates in CRC cells. The up-regulation of XAF1 distinctly increased apoptosis in CRC cells administered by cisplatin (P < 0.001). The XAFl could promoted apoptosis and enhanced chemotherapy sensitivity to cisplatin in CRC cells.