NAPSB as a predictive marker for prognosis and therapy associated with an immuno-hot tumor microenvironment in hepatocellular carcinoma.

BACKGROUND: Napsin B Aspartic Peptidase, Pseudogene (NAPSB) was associated with CD4 + T cell infiltration in pancreatic ductal adenocarcinoma. However, the biological role of NAPSB in hepatocellular carcinoma (HCC) remains to be determined. METHODS: The expression of NAPSB in HCC as well as its clinicopathological association were analyzed using data from several public datasets. qRT-PCR was used to verify the relative expression of NAPSB in patients with HCC using the Zhongnan cohort. Kaplan-Meier analyses, and univariate and multivariate Cox regression were conducted to determine the prognosis value of NAPSB on patients with HCC. Then enrichment analyses were performed to identify the possible biological functions of NAPSB. Subsequently, the immunological characteristics of NAPSB in the HCC tumor microenvironment (TME) were demonstrated comprehensively. The role of NAPSB in predicting hot tumors and its impact on immunotherapy and chemotherapy responses was also analyzed by bioinformatics methods. RESULTS: NAPSB was downregulated in patients with HCC and high NAPSB expression showed an improved survival outcome. Enrichment analyses showed that NAPSB was related to immune activation. NAPSB was positively correlated with immunomodulators, tumor-infiltrating immune cells, T cell inflamed score and cancer-immunity cycle, and highly expressed in immuno-hot tumors. High expression of NAPSB was sensitive to immunotherapy and chemotherapy, possibly due to its association with pyroptosis, apoptosis and necrosis. CONCLUSIONS: NAPSB was correlated with an immuno-hot and inflamed TME, and tumor cell death. It can be utilized as a promising predictive marker for prognosis and therapy in HCC.

[Pathogenesis and clinical significance of interleukin-8 and tumor necrosis factor-alpha in cervicitis].

OBJECTIVE: To investigate the relationship between local immune status of vagina and the occurrence of disease in patients with cervicitis. METHODS: ELISA were used to detect the level of interleukin (IL)-8 and tumor necrosis factor (TNF)alpha in vaginal douche of patients with cervicitis due to ureaplasma urealyticum, mycoplasma hominis, chlamydia trachomatis, neisseria gonorrhoeae and cervical erosion. RESULTS: Compared with the control group, the level of IL-8 in vaginal douche of patients with mycoplasma hominis cervicitis, chlamydia trachomatis cervicitis and neisseria gonorrhoeae cervicitis was significantly higher and there was significant difference ng/L: 371 +/- 34, 369 +/- 31, 339 +/- 36, vs 341 +/- 32, 338 +/- 33, 316 +/- 24, (all P < 0.01). Comparing the level of IL-8 in vaginal douche of patients with ureaplasma urealyticum cervicitis and cervical erosion with that of control group, there was no statistical difference (all P > 0.05). The level of TNF-alpha in vaginal douche of each group was remarkably higher than that of control group except for patients with cervical erosion. And statistically significant difference was found between them (all P < 0.01). CONCLUSION: With regards to the pathogenesis of cervicitis, local immune mechanism of vagina plays an important role in the occurrence of cervicitis. The role of IL-8 in pathogenesis of mycoplasma hominis cervicitis, chlamydia trachomatis cervicitis and neisseria gonorrhoeae cervicitis is likely to be more important.