Objective To explore and evaluate the association between mitotic spindle organizing protein 2A(MZT2A)and survival prognosis and immunotherapy response of skin cutaneous melanoma(SKCM),based on multiomics data mining.Methods The expression difference and survival prognosis of MZT2A in SKCM were analyzed by the Cancer Genome Atlas database,Genotype-tissue Expression Data,Human Protein Atlas,SUMMER database.The biological function of MZT2A and related enriched pathways were analyzed by David2.The differences of immune infiltrating cells,immune therapy response and immune escape ability between high-and low-MZT2A groups were analyzed and compared by using Tumor Immune Estimation Resource,Tumor Immune Single-cell Hub,Tumor-immune System Interactions database,the Cancer Imaging Archive and Tumor Immune Dysfunction and Exclusion databases.Results The expression of MZT2A gene elevated in a variety of cancers,especially in SKCM.SKCM samples with high expression of MZT2A had a poor overall survival.The expression of MZT2A was negatively correlated with the infiltration of CD8+T cells,CD4+T cells,macrophages,neutrophils and dendritic cells in SKCM tissues.In addition,the higher the expression of MZT2A,the therapeutic response of SKCM were worse to immune checkpoint inhibitors(ICI).Conclusion MZT2A is a novel survival prediction target of SKCM.SKCM patients with high expression of MZT2A have poor response to ICI treatment,which provides a theoretical basis for predicting the survival prognosis and guiding immune targeted therapy of SKCM.

Objective To explore and evaluate the association between mitotic spindle organizing protein 2A(MZT2A)and survival prognosis and immunotherapy response of skin cutaneous melanoma(SKCM),based on multiomics data mining.Methods The expression difference and survival prognosis of MZT2A in SKCM were analyzed by the Cancer Genome Atlas database,Genotype-tissue Expression Data,Human Protein Atlas,SUMMER database.The biological function of MZT2A and related enriched pathways were analyzed by David2.The differences of immune infiltrating cells,immune therapy response and immune escape ability between high-and low-MZT2A groups were analyzed and compared by using Tumor Immune Estimation Resource,Tumor Immune Single-cell Hub,Tumor-immune System Interactions database,the Cancer Imaging Archive and Tumor Immune Dysfunction and Exclusion databases.Results The expression of MZT2A gene elevated in a variety of cancers,especially in SKCM.SKCM samples with high expression of MZT2A had a poor overall survival.The expression of MZT2A was negatively correlated with the infiltration of CD8+T cells,CD4+T cells,macrophages,neutrophils and dendritic cells in SKCM tissues.In addition,the higher the expression of MZT2A,the therapeutic response of SKCM were worse to immune checkpoint inhibitors(ICI).Conclusion MZT2A is a novel survival prediction target of SKCM.SKCM patients with high expression of MZT2A have poor response to ICI treatment,which provides a theoretical basis for predicting the survival prognosis and guiding immune targeted therapy of SKCM.

Aim To investigate the effect of baicalin on cell proliferation and cell migration in human skin SCC A431 cell line. Methods The A431 cells were incu-
bated with 50 mg·L-1 baicalin. The protein level of cofilin-1 was assayed by Western blot. Cofilin-1 specific siRNA fragment was designed , synthesized and trans-
fected into A431 cells. The proliferative activity and migration ability of cells were assessed by CCK8 assay and scratch wound healing assay separately. ResultsWestern blot results showed that baicalin treatment in-hibited the cofilin-1 protein expression to 49.3% com-pared with the control group. Single baicalin treatment and cofilin-1 silencing could drease the A431 cell growth and migration. And cofilin-1 silencing signifi-
cantly enhanced the efficacy of baicalin. Conclusions Baicalin could significantly inhibit the tumor cell's growth and migration in the A431 cell line. And cofi-lin-1 might become the potential target gene to enhance the effect of anticancer drugs.

ObjectiveTo investigate baicalin effect against ultraviolet A (UVA) induced senescence in cultured human skin fibroblasts(HSF) and influence on telomere pathway. MethodsHSF were isolated from the prepuce of neonates and cultured. Subconfluent fibroblasts were classified into blank control group (without treatment), baicalin group (treated with baicalin of 50 μg/ml), UVA group (irradiated with UVA of 10 J/cm2) and UVA + baicalin group(irradiated with UVA of 10 J/cm2 and treated with baicalin of 50 μg/ml before and after the irradiation). After additional culture of various durations, flow cytometry was performed to detect cell cycle, telomere repeat amplification protocol-enzyme linked immunosorbent assay (TRAP-ELISA) to measure telomerase activity, real-time quantitative PCR to determine telomere length, mRNA levels of p53, p16 and c-myc, Western blot to examine the protein expressions of p16 and c-myc. ResultsUVA irradiation induced cell cycle arrest in G1 phase, and the percentage of HSF at G1 phase increased from 59.94％ in the blankcontrol group to 81.04％ in the UVA group, but was decreased to 65.55％ in the UVA + baicalin group. The length of telomere in HSF in UVA group was shortened to 31.2％ of that in the blank control group, but was restored to 63.9％ in HSF treated with baicalin before and after the irradiation. Compared with the blank control group, the expression level of p53 and p16 mRNA was increased to 2.93 ± 0.21 and 2.14 ± 0.09, respectively, while that of c-myc mRNA decreased to 0.53 ± 0.03 in the UVA group; baicalin could inhibit these changes. Similarly, Western blot showed that after UVA irradiation the protein expression level of p16 increased to 5.84 ± 0.16, while that of c-myc decreased to 0.35 ± 0.04 in HSF compared with that in the blank control group; baicalin treatment before and after the irradiation induced no significant changes in the protein expres sion of c-myc, but a decline in that of p16 (4.09 ± 0.13, P ＜ 0.05). Telomerase activity was undetected in any of these groups. ConclusionsBaicalin can delay the photoaging process of HSF, which may be attributed to the regulation of expression of senescence-related genes such as p53, but not to telomerase activity.