lncRNA TMEM161B-AS1 screened the onset of oral squamous cell carcinoma in HPV-infected patients, predicted poor prognosis, and regulated cell progression via modulating the miR-651-5p/BDNF axis.

Oral squamous cell carcinoma (OSCC) has become the most common HPV-related cancer with high invasion and metastasis. Exploring biomarkers for the screening and monitoring of OSCC, especially for the HPV-OSCC, would benefit patients' diagnosis and prognosis. This study evaluated the significance and mechanism of TMEM161B-AS1 and miR-651-5p in HPV-OSCC aiming to provide novel insight into the mechanism of HPV-OSCC development. Expression of TMEM161B-AS1 and miR-561-5p was analyzed in healthy individuals, HPV-infected non-OSCC patients, and HPV-OSCC patients using PCR. Their significance in HPV-OSCC occurrence and prognosis was evaluated by logistic regression, ROC, Kaplan-Meier, and Cox regression analysis. In OSCC cells, CCK8 and Transwell assays were employed for assessing cell growth and metastasis. The luciferase reporter assay and cell transfection were performed to evaluate the regulatory association between TMEM161B-AS1, miR-561-5p, and BDNF. Significant upregulation of TMEM161B-AS1 and downregulation of miR-561-5p were observed in oral HPV-infected patients. Both TMEM161B-AS1 and miR-651-5p served as risk factors for the occurrence of OSCC in oral HPV-infected patients and could distinguish HPV-OSCC patients from HPV-infected non-OSCC patients. Increased TMEM161B-AS1 and reduced miR-561-5p indicated severe development and adverse prognosis of HPV-OSCC patients. In OSCC cells, silencing TMEM161-AS1 suppressed cell proliferation and motility via negatively modulating miR-561-5p. miR-561-5p negatively regulated BDNF, which was considered the underlying mechanism of TMEM161B-AS1. Increasing TMEM161B-AS expression and decreasing miR-561-5p showed the occurrence of OSCC in HPV-infected patients and predicted malignant development and adverse prognosis. TMEME161B-AS1 served as a tumor promoter via regulating the miR-561-5p/BDNF axis.

Endothelial cell protein C receptor promotes MGC803 gastric cancer cells proliferation and migration by activating ERK1/2.

The endothelial cell protein C receptor (EPCR) has been reported to be involved in the development of several human cancers. However, the role of EPCR in gastric cancer progression has not been clarified. In this study, we show for the first time that EPCR is related to gastric cancer. Our results indicate that EPCR is highly expressed in clinical gastric cancer tissue. Knockdown of EPCR by small interference RNA suppressed the proliferation and migration of MGC803 gastric cancer cells dominantly. Blocking antibodies to protease-activated receptor-1(PAR1) also suppressed the proliferation and migration of MGC803 cells. Knockdown EPCR and blocking PAR1 inhibit activation of extracellular signaling-regulated kinases 1 and 2 (ERK1/2). Taken together, these results indicate that EPCR contributes to the proliferation and migration of MGC803 gastric cancer cells by activating ERK1/2, and this effect of EPCR may be dependent on PAR1. Therefore, EPCR may be act as a novel therapeutic target for inhibiting cell growth in gastric cancer.