The Context-Dependent Impact of Integrin-Associated CD151 and Other Tetraspanins on Cancer Development and Progression: A Class of Versatile Mediators of Cellular Function and Signaling, Tumorigenesis and Metastasis

As a family of integral membrane proteins, tetraspanins have been functionally linked to a wide spectrum of human cancers, ranging from breast, colon, lung, ovarian, prostate, and skin carcinomas to glioblastoma. CD151 is one such prominent member of the tetraspanin family recently suggested to mediate tumor development, growth, and progression in oncogenic context- and cell lineage-dependent manners. In the current review, we summarize recent advances in mechanistic understanding of the function and signaling of integrin-associated CD151 and other tetraspanins in multiple cancer types. We also highlight emerging genetic and epigenetic evidence on the intrinsic links between tetraspanins, the epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs), and the Wnt/β-catenin pathway, as well as the dynamics of exosome and cellular metabolism. Finally, we discuss the implications of the highly plastic nature and epigenetic susceptibility of CD151 expression, function, and signaling for clinical diagnosis and therapeutic intervention for human cancer

Intravenous flurbiprofen axetil can increase analgesic effect in refractory cancer pain

<p>Abstract</p> <p>Background</p> <p>The aim of this study was to investigate the analgesic effects of intravenous flurbiprofen axetil for the refractory pain in cancer patients.</p> <p>Methods</p> <p>2109 patients were screened from the department of medical oncology, the first affiliated hospital of Anhui medical university in China between October of 2007 and October of 2008. Thirty-seven cases of cancer patients who had bad effect from anaesthetic drugs were received administration of intravenous flurbiprofen axetil with dose of 50 mg/5 ml/day. The pain score was evaluated for pre- and post- treatment by Pain Faces Scale criteria, and the side effects were also observed.</p> <p>Results</p> <p>Intravenous flurbiprofen axetil increased the analgesic effects. The total effective rate was 92%. The side effects, such as abdominal pain, alimentary tract bleeding which were found in using NSAIDs or constipation, nausea, vomit, sleepiness which were found in using opioid drugs did not be found.</p> <p>Conclusion</p> <p>Intravenous flurbiprofen axetil could provide better analgesia effects and few side effects to patients with refractory cancer pain. It could also increase analgesia effects when combining with anesthetic drugs in treatment of moderate or severe pain, especially breakthrough pain, and suit to patients who can not take oral drugs for the reason of constipation and psychosomatic symptoms.</p

MiR–20a-5p promotes radio-resistance by targeting Rab27B in nasopharyngeal cancer cells

Additional file 3: Figure S2. The protein level of PARP and caspase3 detected by western in NCM, 5PM, NCA, 5PA, si-NC and si-Rab27B transfected CNE-2 and CNE-1 cells respectively

An autophagic gene‐based signature to predict the survival of patients with low‐grade gliomas

Abstract Background Since autophagy remains an important topic of investigation, the RNA‐sequence profiles of autophagy‐related genes (ARGs) can provide insights into predicting low‐grade gliomas (LGG) prognosis. Methods The RNA‐seq profiles of autophagic genes and prognosis data of LGG were integrated from the Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA). Univariate Cox analysis and the least absolute shrinkage and selection operator (LASSO) regression model were carried out to identify the differentially expressed prognostic autophagy‐related genes. Then, the autophagic‐gene signature was formed and verified in TCGA test set and external CGGA cohorts. Time‐dependent receiver operating characteristic (ROC) was examined to test the accuracy of this signature feature. A nomogram was conducted to meet the needs of clinicians. Sankey diagrams were performed to visualize the relationship between the multigene signatures and clinic‐pathological features. Results Twenty‐four ARGs were finally identified most relevant to LGG prognosis. According to the specific prediction index formula, the patients were classified into low‐risk or high‐risk groups. Prognostic accuracy was proved by time‐dependent ROC analysis, with AUC 0.9, 0.93, and 0.876 at the survival time of 2‐, 3‐, and 5‐year, respectively, which was superior to the AUC of the isocitrate dehydrogenase (IDH) mutation. The result was confirmed while validated in the TCGA test set and external validation CGGA cohort. A nomogram was constructed to meet individual needs. With a visualization approach, Sankey diagrams show the relationship of the histological type, IDH status, and predict index. In TCGA and CGGA cohorts, both low‐risk groups displayed better survival rate in LGG while histological type and IDH status did not show consistency results. Conclusions 24‐ARGs may play crucial roles in the progression of LGG, and LGG patients were effectively divided into low‐risk and high‐risk groups according to prognostic prediction. Overall, our study will provide novel strategies for clinical applications

FOXA1‐induced LINC00621 promotes lung adenocarcinoma progression via activating the TGF‐β signaling pathway

Abstract Background Lung adenocarcinoma (LUAD) is highly malignant and associated with poor prognoses in patients worldwide. There has been widespread recognition that lncRNAs are tightly linked to LUAD tumorigenesis and development. Here, we identified that the LINC00621 level was increased in LUAD tissues and concerned with the poor prognoses in LUAD patients. Methods Bioinformatical analysis and RT‐qPCR determined the level of LINC00621 in LUAD tissues and cell lines. The admeasurement of the proliferation, migration, and invasion abilities of LUAD cells was utilized in the CCK8 and Transwell formulas. Luciferase reporter assay was used to corroborate the downstream target genes of LINC00621. The phosphorylated SMAD3 protein was tested by Western blotting assay. The impression of LINC00621 knockdown on LUAD tumor growth and metastasis put into effect by murine models. ChIP‐qPCR assay was carried out to verify the transcriptional regulation by FOXA1 on LINC00621. Results In vitro, the knockdown of LINC00621 significantly reduced the proliferative, migrating, and invasive abilities, the same was true for tumorigenesis and metastasis in vivo. MiR‐34a‐5p as a straight target of LINC00621 was ascertained, and LUAD patients with inferior miR‐34a‐5p levels had undesirable prognoses. Furthermore, TGFBR1 is an immediate and functional connection site of miR‐34a‐5p. Collectively, LINC00621 can sponge miR‐34a‐5p and upregulate TGFBR1 levels, which further sensitized TGF‐β signaling pathway. Finally, it was revealed that FOXA1 transcriptionally upregulated LINC00621. Conclusion This study uncovered that FOXA1‐induced LINC00621 promotes LUAD progression via the miR‐34a‐5p/TGFBR1/TGF‐β axis, and is one novel therapeutic target that may be used in LUAD treatment