Purpose: The aim of this study is to investigate the differential expression of α-sma-positive fibroblasts (CAFs) in nasopharyngeal carcinomas (NPCs), nasopharyngitis, metastatic tissues of NPCs and its prognostic value in NPCs.Methods: The expression of α-sma-labeled CAFs in 85 NPCs, 32 nasopharyngitis and 12 metastatic tissues of NPCs was detected by immunohistochemical method. The relationship between CAFs and clinicopathological parameters of NPCs was analyzed.Results: The high density of CAFs in the NPCs, nasopharyngitis and metastatic tissues of NPCs group were 41.2% (35/85), 6.2% (2/32) and 83.3% (10/12), and a significant difference was showed among these three groups (P<0.05). Chi-square test showed that there was no significant correlation between the density of CAFs and gender, age, N stage, treatment (P>0.05), but closely correlated with T stage and relapse (P<0.05). Kaplan-Meier survival analysis showed that the mean overall survival of high-density and low-density CAFs was 86.8 months and 127.0 months, respectively. Correspondingly, the 5-year survival rates were 57.1% (20/35) and 90.0% (45/50), and there were inversely statistical differences between two groups (P<0.05). Cox multivariate analysis showed that the density of CAFs could be used as an independent prognostic factor for the survival of NPC patients (P<0.05).Conclusions: The density of CAFs could be closely related to the metastasis of NPCs, and also is an efficient prediction factor of poor survival in patients with NPCs.

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Bladder cancer (BLCA) is a common genitourinary cancer in patients, and tumour angiogenesis is indispensable for its occurrence and development. However, the indepth mechanism of tumour angiogenesis in BLCA remains elusive. According to recent studies, the tight junction protein family member occludin (OCLN) is expressed at high levels in BLCA tissues and correlates with a poor prognosis. Downregulation of OCLN inhibits tumour angiogenesis in BLCA cells and murine xenografts, whereas OCLN overexpression exerts the opposite effect. Mechanistically, the RT-qPCR analysis and Western blotting results showed that OCLN increased interleukin-8 (IL8) and p-signal transducer and activator of transcription 3 (STAT3) levels to promote BLCA angiogenesis. RNA sequencing analysis and dual-luciferase reporter assays indicated that OCLN regulated IL8 transcriptional activity via the transcription factor STAT4. In summary, our results provide new perspectives on OCLN, as this protein participates in the development of BLCA angiogenesis by activating the IL8/STAT3 pathway via STAT4 and may serve as a novel and unique therapeutic target.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive tumors, characterized by diagnosis at an advanced stage and a poor prognosis. As a member of the S100 protein family, S100A10 regulates multiple biological functions related to cancer progression and metastasis. However, the role of S100A10 in PDAC is still not completely elucidated. In this study, we reported that S100A10 was significantly up-regulated in PDAC tissue and associated with a poor prognosis by integrated bioinformatic analysis and human PDAC tissue samples. In vitro, down-regulation of S100A10 reduced the proliferation, migration, and adhesion of PDAC cell lines, whereas up-regulation of S100A10 showed the opposite effect. Furthermore, LAMB3 was proved to be activated by S100A10 using RNA-sequencing and western blotting. The effect of LAMB3 on the proliferation, migration, and adhesion of PDAC cells was similar to that of S100A10. Up-regulation or down-regulation of LAMB3 could reverse the corresponding effect of S100A10. Moreover, we validated S100A10 activates LAMB3 through the JNK pathway, and LAMB3 was further proved to interact with LAMC2. Mice-bearing orthotopic pancreatic tumors showed that S100A10 knocked-down PANC-1 cells had a smaller tumor size than the control group. In conclusion, S100A10 promotes PDAC cells proliferation, migration, and adhesion through JNK/LAMB3-LAMC2 axis.