The homolog of p53 gene, p63, encodes multiple p63 protein isoforms. TAp63 proteins contain an N-terminal transactivation domain similar to that of p53 and function as tumor suppressors; whereas ΔNp63 isoforms, which lack the intact N-terminal transactivation domain, are associated with human tumorigenesis. Accumulating evidence demonstrating the important roles of p63 in development and cancer development, the regulation of p63 proteins, however, is not fully understood. In this study, we show that peptidyl-prolyl isomerase Pin1 directly binds to and stabilizes TAp63α and ΔNp63α via inhibiting the proteasomal degradation mediated by E3 ligase WWP1. We further show that Pin1 specifically interacts with T538P which is adjacent to the P550PxY543 motif, and disrupts p63α–WWP1 interaction. In addition, while Pin1 enhances TAp63α-mediated apoptosis, it promotes ΔNp63α-induced cell proliferation. Furthermore, knockdown of Pin1 in FaDu cells inhibits tumor formation in nude mice, which is rescued by simultaneous knockdown of WWP1 or ectopic expression of ΔNp63α. Moreover, overexpression of Pin1 correlates with increased expression of ΔNp63α in human oral squamous cell carcinoma samples. Together, these results suggest that Pin1-mediated modulation of ΔNp63α may have a causative role in tumorigenesis.

Context: Dendrobium officinale Kimura et Migo (Orchidaceae) is a naturally occurring precious traditional Chinese medicine (TCM) originally used in treating yin-deficiency diseases. The main active substances of Dendrobium officinale are polysaccharides (DOP). Recent findings highlighted the potential of DOP as a promising natural material for medical use with a diversity of pharmaceutical effects. Objective: In this review, we provide a systematic discussion of the current development and potential pharmacological effects of Dendrobium officinale polysaccharides in dermatology. Methods: English and Chinese literature from 1987 to 2019 indexed in databases including PubMed, PubMed Central, Web of Science, ISI, Scopus and CNKI (Chinese) was used. Dendrobium officinale, Dendrobium officinale polysaccharides, phytochemistry, chemical constituents, biological activities, and pharmacological activities were used as the key words. Results: Dendrobium officinale polysaccharides have been found to possess hair growth promoting, skin moisturising and antioxidant effects, which are highly valued by doctors and cosmetic engineers. We highlighted advances in moisturising and antioxidant properties from in vivo and in vitro studies. Dendrobium officinale polysaccharides exhibited strong antioxidant effects by decreasing free radicals, enhancing antioxidant system, inhibiting nuclear factor-kappa B and down-regulating inflammatory response. Conclusions: Our review is a foundation to inspire further research to facilitate the application of Dendrobium officinale polysaccharides in dermatology and promote active research of the use of TCM in dermatology.

Acquired immune deficiency syndrome (AIDS), which is caused by HIV infection, is an epidemic disease that has killed millions of people in the last several decades. Although combination antiretroviral therapy (cART) has enabled tremendous progress in suppressing HIV replication, it fails to eliminate HIV latently infected cells, and infected individuals remain HIV positive for life. Lifelong antiretroviral therapy is required to maintain control of virus replication, which may result in significant problems, including long-term toxicity, high cost, and stigma. Therefore, novel therapeutic strategies are urgently needed to eliminate the viral reservoir in the host for HIV cure. In this review, we compare several potential strategies regarding HIV cure and focus on how we might utilize chimeric antigen receptor-modified T cells (CAR T) as a therapy to cure HIV infection.

Tripartite motif 16 (TRIM16), a member of the RING B-box coiled-coil (RBCC)/tripartite motif (TRIM) protein family, has been shown to play a role in tumor development and progression. However, the role of TRIM16 in ovarian cancer has never been revealed. Thus, in this study, we investigated the roles and mechanisms of TRIM16 in ovarian cancer. Our results demonstrated that TRIM16 expression was low in ovarian cancer cell lines. In addition, overexpression of TRIM16 significantly inhibited the migration and invasion in vitro, as well as suppressed the epithelial-mesenchymal transition (EMT) phenotype in ovarian cancer cells. Furthermore, overexpression of TRIM16 greatly inhibited the protein expression levels of Shh, Smo, Ptc, Gli-1, MMP2, and MMP9 in ovarian cancer cells. Taken together, these results strongly suggest that TRIM16 inhibits the migration and invasion via suppressing the Sonic hedgehog signaling pathway in ovarian cancer cells. Thus, TRIM16 may be a novel potential therapeutic target for ovarian cancer.