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Oligomers of benzoylalanine-based amidothioureas containing four β-turn structures spaced by meta-substituted benzenes were shown to undergo assembly in dilute CH3CN solution into supramolecular helices of enhanced supramolecular helicity, whereas those spaced by para-substituted benzene spacer(s) or those spaced by meta-substituted benzenes but with one or two β-turns exhibit a substantially decreased tendency of assembling. [ABSTRACT FROM AUTHOR]

Renal interstitial fibrosis (RIF) represents an irreversible and progressive pathological manifestation of chronic renal disease, which ultimately leads to end‐stage renal disease. Long noncoding RNAs (lncRNAs) have been suggested to be involved in the progression of RIF. Small nucleolar RNA host gene 16 (SNHG16), a member of lncRNAs, has been found to be involved in the progression of pulmonary fibrosis. This paper first researched the effect of SNHG16 on renal fibrosis. We established a unilateral ureteral obstruction (UUO)‐induced mouse RIF model by ligation of the left ureter to evaluate the biological function of SNHG16 in RIF. As a result, SNHG16 was upregulated in UUO‐induced renal fibrotic tissues. Knockdown of SNHG16 inhibited RIF and reduced alpha‐smooth muscle actin (α‐SMA), fibronectin, and college IV expression. miR‐205 was a target of SNHG16, and downregulated in UUO‐induced renal fibrotic tissues. Inhibition of miR‐205 promoted RIF and increased the expression of α‐SMA, college IV, and fibronectin. Overexpression of SNHG16 promoted the UUO‐induced RIF, but miR‐205 abrogated this effect of SNHG16. Histone deacetylase 5 (HDAC5) showed high expression in UUO‐induced renal fibrotic tissues. Knockdown of HDAC5 significantly reduced α‐SMA, fibronectin, and college IV expression in renal tissues of UUO‐induced mice. Inhibition of miR‐205 promoted HDAC5 expression, but knockdown of SNHG16 inhibited HDAC5 expression in renal tissues of UUO‐induced mice. In conclusion, SHNG16 is highly expressed in renal fibrotic tissues of UUO‐induced mice. Knockdown of SHNG16 may prevent UUO‐induced RIF by indirectly upregulating HDAC5 via targeting miR‐205. SHNG16 may be novel target for treating renal fibrosis. [ABSTRACT FROM AUTHOR]

Ovarian cancer is the leading cause of death from female gynecological cancers. Cisplatin (DDP) is a first-line drug for ovarian cancer treatment. Due to DDP resistance, there is an urgent need for novel therapeutic drugs with improved antitumor activity. AMPK-mediated metabolic regulatory pathways are related to tumor drug resistance. Our study aimed to determine the relationship between reversing DDP resistance with the anthraquinone derivative KA-4s and regulating AMPK energy metabolism in ovarian cancer. The results showed that KA-4s inhibited the proliferation of ovarian cancer cells. The combination of KA-4s with DDP effectively promoted drug-resistant ovarian cancer cell apoptosis and inhibited cell migration and invasion. Moreover, KA-4s decreased the intracellular ATP level and increased the calcium ion level, leading to AMPK phosphorylation. Further studies suggested that the AMPK signaling pathway may be involved in the mechanism through which KA-4s reduce drug resistance. KA-4s inhibited mitochondrial respiration and glycolysis; downregulated the glucose metabolism-related proteins GLUT1 and GLUT4; the lipid metabolism-related proteins SREBP1 and SCD1; and the drug resistance-related proteins P-gp, MRP1, and LRP. The inhibitory effect of KA-4s on GLUT1 was confirmed by the application of the GLUT1 inhibitor BAY-876. KA-4s combined with DDP significantly increased the expression of p-AMPK and reduced the expression of P-gp. In a xenograft model of ovarian cancer, treatment with KA-4s combined with DDP reduced energy metabolism and drug resistance, inducing tumor apoptosis. Consequently, KA-4s might be evaluated as a new agent for enhancing the chemotherapeutic efficacy of treatment for ovarian cancer., (© 2024 Wiley Periodicals LLC.)