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Skin cutaneous melanoma has high morbidity and mortality. Identification of reliable and quantitative melanoma biomarkers could facilitate an early diagnosis and improve survival and morbidity rates. CD96 has a significant role in adjusting immune function. Although the abnormal expression of CD96 has been reported to participate in carcinogenesis in many human types of cancer, the bioinformatics role of the CD96 in melanoma is unknown. Expression degrees and their underlying functions were first studied by this study. According to TCGA, GTEx, and gene expression profile interaction analysis dataset in this paper, compared with normal skin tissues, CD96 was expressed at higher levels in human cutaneous melanoma skin tissues. Meanwhile, we detected the relative CD96 expression levels by immunohistochemistry. Gene functional enrichment analyses were applied through cBioPortal database analysis. CD96 was clearly upregulated in skin cutaneous melanoma patients and carried out its effects through regulating several signaling pathways, containing the JAK-STAT, PI3K-Akt, and MAPK. Taken together, the analysis results indicated that CD96 could be used as a new clinical bioindicator as well as an underlying medicinal target for cutaneous melanoma.

As one of the most aggressive malignancies, cervical cancer (CC) which mainly affects females has high risks of relapse and death. Long non-coding RNA (lncRNA) RP11-552M11.4 is verified to promote the progression of ovarian cancer; nevertheless, its role and the probable molecular mechanisms in CC remain unclear until the present study. Herein, we unveiled that the expression of lncRNA RP11-552M11.4 tested by qRT-PCR was enhanced in tumor tissues compared with the para-carcinoma tissues and related to FIGO Stage, lymph node metastasis, vascular invasion and distant metastasis in CC. Additionally, CC patients with high lncRNA RP11-552M11.4 level suffered from poor clinical outcomes. Moreover, silenced lncRNA RP11-552M11.4 restrained cell proliferation, migration and invasion in CC cells. Subsequently, the mechanistic studies revealed that lncRNA RP11-552M11.4 functioned as a ceRNA of ATF1 in CC by acting as the endogenous sponge for miR-3941, which was identified as a tumor suppressor in CC. Moreover, both miR-3941 inhibition and ATF1 overexpression restored the impacts of inhibited lncRNA RP11-552M11.4 on cellular processes in CC cells. Our observations elucidated the carcinogenic role of lncRNA RP11-552M11.4 in CC was mediated through miR-3941/ATF1 axis, giving a new insight into the effective target for the treatment and prognosis of cervical cancer.