The presence of autoantibodies as a potential prognostic biomarker for breast cancer.

The presence of autoantibodies is closely associated with the occurrence and development of cancer. Autoantibodies can be used as biomarkers for early breast cancer diagnosis. However, the relationship between autoantibodies and the prognosis of breast cancer patients remains elusive. This retrospective study aimed to investigate the correlation between the presence of autoantibodies and outcomes in breast cancer patients. This study included a total of 155 patients from People's Hospital of Henan University (Zhengzhou, China) who were diagnosed with breast cancer from January 2017 to December 2021. The enrolled patients' clinicopathological features were collected, and 88 patients were ultimately involved in the analysis. Univariate and multivariate Cox regression analyses were performed to search for the risk factors related to the poor prognosis of breast cancer patients. The association between the presence of autoantibodies and patients' survival was analysed using Kaplan-Meier curves. After screening, there were 38 autoantibody-positive cases and 50 autoantibody-negative cases. Breast cancer patients with autoantibody-positive had a 57% lower risk of death compared with autoantibody-negative patients. Multivariate Cox regression analysis indicated that the presence of autoantibody could be a potential prognostic predictor for breast cancer, independent of age, histological grade, pathological classification, clinical stage, and the expression levels of hormonal receptors. In addition, autoantibody-positive breast cancer patients had longer progression-free survival and overall survival compared with autoantibody-negative cases. Positive autoantibody was found as an independent biomarker of better prognosis in breast cancer patients, providing a new strategy for the prognostic assessment of breast cancer patients.

PLCε promotes the Warburg effect and tumorigenesis through AKT/GSK3ß/Cdc25a in bladder cancer.

Phospholipase C epsilon (PLCε) is a oncogene in various malignancies and regulates diverse cellular functions. But understanding of the relation between PLCε and glycolytic pathways has not been clearly identified. In the present study, we explored the effect of PLCε on the Warburg effect and tumorigenesis in bladder cancer (BCa). In our study, we showed that PLCε expression was elevated in BCa samples compared with matched adjacent nonmalignant bladder tissues. PLCε depletion using Lentivirus-shPLCε (LV-shPLCε) dramatically decreased cell growth, glucose consumption and lactate production, arresting T24 and BIU cells in the S phase of the cell cycle. We also observed that PLCε was correlated with the activation of protein kinase B (AKT) and cell division cycle 25 homolog A (Cdc25a) overexpression. In addition, we demonstrated that AKT/glycogen synthase kinase 3 beta (GSK3ß)/Cdc25a signaling pathways are involved in the PLCε-mediated Warburg effect in BCa. Moreover, we showed that PLCε had an effect on tumorigenesis in in vivo experiments. In summary, our findings demonstrate that AKT/GSK3ß/Cdc25a is critical for the effect PLCε on Warburg effect and tumorigenesis.

Upregulated lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/ß-catenin signaling pathway.

Lung cancer is the most common and aggressive tumor in the world. Long non-coding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) play critical roles in the progression of cancers. However, the function and underlying mechanism remain unclear in lung cancer. In the current study, we found that expression of SNHG1 was up-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines. NSCLC patients with high SNHG1 expression were significantly correlated with larger tumor size, advanced TNM stage, lymph node metastasis and poor overall survival than patients with low SNHG1 expression. Furthermore, function assays showed that SNHG1 inhibition suppressed NSCLC cell proliferation both in vitro and in vivo. We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p. In addition, we identified that SOX9 acted as a target of miR-101-3p, and SOX9 played the oncogenic role in NSCLC by activating Wnt/ß-catenin signaling pathway. Taken together, our study suggested that lncRNA SNHG1 could promote NSCLC progression via miR-101-3p and SOX9. The SNHG1/miR-101-3p/SOX9/Wnt/ß-catenin axis regulatory network might provide a potential new therapeutic strategy for lung cancer treatment.