The promotive role of lncRNA MIR205HG in proliferation, invasion, and migration of melanoma cells via the JMJD2C/ALKBH5 axis.

Melanoma is a highly malignant skin cancer. This study aimed to investigate the role of long non-coding RNA MIR205 host gene (lncRNA MIR205HG) in proliferation, invasion, and migration of melanoma cells via jumonji domain containing 2C (JMJD2C) and ALKB homolog 5 (ALKBH5). Real-time quantitative polymerase chain reaction or Western blot assay showed that MIR205HG, JMJD2C, and ALKBH5 were increased in melanoma cell lines. Cell counting kit-8, colony formation, and Transwell assays showed that silencing MIR205HG inhibited proliferation, invasion, and migration of melanoma cells. RNA immunoprecipitation, actinomycin D treatment, and chromatin immunoprecipitation showed that MIR205HG may bind to human antigen R (HuR, ELAVL1) and stabilized JMJD2C expression, and JMJD2C may increase the enrichment of H3K9me3 in the ALKBH5 promotor region to promote ALKBH5 transcription. The tumor xenograft assay based on subcutaneous injection of sh-MIR205HG-treated melanoma cells showed that silencing MIR205HG suppressed tumor growth and reduced Ki67 positive rate by inactivating the JMJD2C/ALKBH5 axis. Generally, MIR205HG facilitated proliferation, invasion, and migration of melanoma cells through HuR-mediated stabilization of JMJD2C and increasing ALKBH5 transcription by erasing H3K9me3.

Acitretin modulates HaCaT cells proliferation through STAT1- and STAT3-dependent signaling.

Acitretin has been a valuable option for the treatment of psoriasis, however, the molecular events of acitretin leading to the normalization of keratinocytes differentiation on psoriasis patients have not been fully explored. To investigate whether there were certain relationship between keratinocytes proliferation and JAK/STAT signaling pathways in psoriasis, and how acitretin modulated the signaling pathways. HaCaT cells, an in vitro immortal human keratinocyte cell line, was chosen as a in vitro model of psoriasis. The small interfering RNA targeting STAT1 (siRNA-STAT1) and STAT3 (siRNA-STAT3) were subsequently transfected into the HaCaT cells which were treated with or without acitretin. We found that HaCaT cells proliferation and the expression of STAT1 or STAT3 were inhibited by acitretin, siRNA-STAT1 and siRNA-STAT3. Our experimental data shows that acitretin might inhibit HaCaT cells proliferation in psoriasis by decreasing the expression of STAT- and STAT3-dependent mechanism.

Systemic lupus erythematosus patient with false positive results of antibody to HIV: A case report and a comprehensive literature review.

A 76-year-old woman has got both lower limbs petechia and ecchymosis for 1 month, edema for 6 days and fever for 3 days. The patient suffered from purpura of both lower limbs, edema, arthralgia, recurrent fever, kidney damages, serositis, progressive reduction of platelet, moderate anemia and lymphadenopathy during the last two months. Laboratory examinations showed that her whole blood cells, platelet counts, serum albumin level and complements were all decreased and her titres of antibodies to double-stranded DNA (ds-DNA) were high. The patient had unequivocal SLE as she fulfilled seven American Rheumatism Association criteria (1997). Enzyme linked immunosorbent assays (ELISAs) for human immunodeficiency virus (HIV) was positive, while negative by Western blot analysis. A diagnosis of Systemic lupus erythematosus was made in view of the above findings. Because of the presence of autoantibodies and cross-reactivity, diagnosis of HIV infection should be cautious in patients with systemic autoimmune disease. The use of rigorous confirmatory testing by western blot analysis or immunofluorescence assay is therefore mandatory. More sensitive assays may be necessary to confirm the presence of HIV infection, such as gene amplification by the polymerase chain reaction, virus isolation and cultivation, the CD4 cell count and the ratio of CD4/CD8.