Curcumin is a polyphenolic natural compound with diverse and attractive biological activities, which may prevent or ameliorate pathological processes underlying age‐related cognitive decline, dementia, or mood disorders. However, clinical trials and animal studies have yielded conflicting conclusions regarding its effectiveness for cognition in different individuals. The aim of this review is to meta‐analytically assess the effectiveness of curcumin for cognitive function in different types of people. A preliminary search on PubMed, Embase, Web of Science, ClinicalTrials.gov, Cochrane Library, Chinese National Knowledge Infrastructure, and Wanfang Data and China Biology Medicine disc was performed to identify randomized controlled trials investigating the effect of curcumin on cognition. Six clinical trials with a total of 289 subjects met inclusion criteria for this review. We used a random‐effects model to calculate the pooled standardized difference of means (SMD). For older adults who received curcumin, scores on measures of cognitive function (SMD = 0.33, 95% confidence interval [CI] [0.05, 0.62]; p = 0.02), occurrence of adverse events (odds ratio [OR] = 5.59, 95% CI [0.96, 36.80]; p = 0.05), and measures of depression (SMD = −0.29, 95% CI [0.64, 0.05]; p = 0.09) indicated significant memory improvement. In patients with Alzheimer's disease (AD), scores in measures of cognition status (SMD = −0.90, 95% CI [1.48, −0.32]; p = 0.002) indicated that there was a trend for treated subjects to do worse than placebo‐treated subjects on the Mini‐Mental State Examination. The occurrence of adverse events (OR = 0.87, 95% CI [0.10, 7.51]; p = 0.90) was similar to those who received placebo. Due to insufficient data, it was impossible to provide a narrative account of only the outcomes for schizophrenia. Curcumin appears to be more effective in improving cognitive function in the elderly than in improving symptoms of AD and schizophrenia. Curcumin is also safe and tolerated among these individuals. Because of the small number of studies available, a funnel plot or sensitivity analysis was not possible. Further high‐quality trials with larger sample sizes or bioavailability‐improved curcumin formulations may be considered for reliable assessment.

Our results suggest that Pin1 plays an important role in tumorigenesis of PCa, suggesting that targeting Pin1 pathway could represent a potential modality for treating PCa.

Aberrant expression of the Cullin 4A (CUL4A) is found in many tumor types, but the functions and mechanism of CUL4A in prostate cancer (PCa) development and progression remain largely unknown. The aim of this study was to investigate the possible role of CUL4A in prostate tumorigenesis. Immunohistochemistry was used to examine CUL4A expression in human PCa tissues and BPH tissues. Cell proliferation was assessed by MTT, and migration and invasion were analyzed by Transwell and Matrigel assays after CUL4A knockdown in PCa in vitro. The results showed that CUL4A protein was overexpressed in 86.21 % of PCa tissues. CUL4A knockdown with siRNA in PCa cells decreased cell proliferation, migration, and invasion. Mechanistically, CUL4A could modulate the expression of P53 in PCa cells. Our results indicate that CUL4A overexpression play an oncogenic role in the pathogenesis of PCa, and CUL4A may be a potential therapeutic target for PCa.

Glioblastoma multiforme is characterized by high invasiveness, multidrug resistance, and inevitable recurrence, and current standard treatment regimens are not curative. Even if most glioma cells are eliminated by chemotherapy and radiotherapy, glioma stem cells can survive and differentiate into new tumor cells, thereby triggering tumor recurrence and drug resistance. Therefore, inhibiting tumor invasiveness, reversing drug resistance, and effectively ablating glioma stem cells are critical for improving the prognosis of glioblastoma multiforme. Previous studies reported that the combination of β-diketone–cobalt complexes (CoAc2) and temozolomide (TMZ) has synergistic inhibitory effects on glioma cells. Therefore, we compared cell proliferation, colony-forming capacity, cell migration, and invasion of TMZ-resistant glioma cells and corresponding glioma stem cells after treatment with CoAc2 and/or TMZ. We also explored the underlying mechanism by which CoAc2 sensitizes cells to TMZ through transcriptome sequencing and related signal pathway blockade. We found that CoAc2 significantly increased the inhibitory effect of TMZ on the proliferation, colony formation, migration, invasion, and survival of drug-resistant stem cells. By downregulating ERK pathway activity, CoAc2 inhibited the expression of O6-methylguanine-DNA methyltransferase and eventually sensitized drug-resistant glioma cells to TMZ. In conclusion, the combined use of CoAc2 and TMZ can reverse TMZ resistance and significantly enhance its inhibitory effect on the malignant phenotype of glioma cells and glioma stem cells.