AQP3 (Aquaporin 3)

We hypothesized that the pan-HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) would improve corneal healing in diabetic mice...In vitro SAHA treatment of human corneal epithelial cells (HCECs) significantly increased protein expression of AQP3, important for corneal wound healing, but had no effect on ROS production. In conclusion, treatment with SAHA improved corneal wound healing, not only in male mice with diabetes and delayed wound healing but also in normoglycemic male mice; therefore, SAHA could potentially be repurposed as a topical treatment clinically to improve corneal wound healing.

AFM-based force spectroscopy demonstrated that AQP1 overexpression increased both cell stiffness and cell-cell adhesion, AQP3 overexpression enhanced cell stiffness but slightly reduced cell-cell adhesion, whereas AQP5 overexpression increased both cell elasticity and cell-cell adhesion. Thus, AQP1, AQP3, and AQP5 may play a crucial role in promoting tumor growth and invasion by differentially modulating cell stiffness and cell-cell adhesion.

Encorelane effectively targets both inflammation and aging signs, supporting its use as a dermocosmetic solution for sensitive, aging-prone skin.

The underlying molecular mechanisms of androgen action were elucidated using AQP3- and AR-specific siRNAs and pharmacological inhibitors. These findings underscore the urgent need to investigate the role of sex hormones in lung cancer and other androgen-responsive epithelial models, focusing on their influence on cancer cell survival and motility.

After compounding with GR and its components, the BCS classification of EPR was unchanged but shifted toward high solubility and low permeability. The findings indicate that GR-EPR could exhibit significant potential in mitigating ascites associated with hepatocellular carcinoma.

Sixty SPF-grade mice were randomly divided into a blank group, a model group, loperamide hydrochloride group (5 mg/kg), a high-dose PG group (100 mg/kg), a medium-dose group (50 mg/kg), and a low-dose group (25 mg/kg), with 10 mice in each group and an equal number of males and females...Compared with the model group, all doses of PG groups reduced the levels of IL-1β, IL-6, and TNF-α in mouse serum (P<0.05), improved pathological changes in the small intestine, increased the content of T-SOD in the small intestine tissue, reduced the content of MDA, increased the expression of AQP4 and AQP8 mRNA, and decreased the expression of AQP3 and NHE8 mRNA (P<0.05), increased the expression of AQP8 protein. PG could improve the pathological changes of chronic enteritis in mice, enhance antioxidant capacity, and alleviate diarrhea caused by chronic enteritis by downregulating the expression of intestinal epithelial transport proteins and acute-phase proteins, and altering gut microbiota.

Consistently, AQP3 knockdown by RNA silencing downregulated its gene expression, leading to a decrease in stemness, EMT and angiogenesis properties in H1299 cells. MP06 could thus serve as a novel therapeutic target with anticancer and angiogenesis properties for non‑small cell lung cancer.

However, the potential translation of AQPs biomarkers into clinical applications is promising and the understanding of the precise mechanisms influencing respiratory diseases is still ongoing. Addressing the challenges and outlining the future perspectives in AQPs development is essential for clinical progress in a concise manner.

Of note, AQP1 overexpression increased cell migration and induced cell detachment and dissemination from migrating breast cancer cell sheets, whereas AQP3 overexpression did not. Thus, AQP1 and AQP3 differentially affect 3D grown breast cancer spheroids and especially AQP1 may contribute to cancer development and spread via negatively affecting cellular junctions and cell polarity proteins as well as increasing cell migration and cell detachment.

A cellular proliferation marker, Ki67, was detected only in the area including basaloid cells in both tumor types. These findings suggest that AQP3 is useful for clarifying the origin of sebaceous gland tumors, and that AQP3 may be related to sebaceous gland development.

In addition, AQP3 can promote the lysis of EBV in EBV-positive NPC cells. The inhibition of AQP3 expression by EBV through LMP1 may be one of the mechanisms by which EBV maintains latent infection-induced tumor progression.

Mixed subcutaneous transplanted tumor mice and Aqp3 knockout mice models were further utilized, and revealed that AQP3 played a critical role in mediating M2 macrophage polarization, modulating glucose metabolism in tumors, and regulating both upstream and downstream pathways. Overall, our study demonstrated that AQP3 could regulate the proliferation, migration, and glycometabolism of tumor cells by modulating M2 macrophages polarization through the PPAR-γ/NF-κB axis and IL-6/IL-6R signaling pathway, providing new insight into the early detection and potential therapeutic target of LUAD.