Spicy foods and chili peppers contain the primary ingredient capsaicin, which has potential health benefits. However, their efficacy in some health outcomes is also fiercely disputed, and some side effects have been confirmed. To assess the quality and strength of the associations between spicy food and chili pepper consumption and different health outcomes. An umbrella review is performed in humans. Eleven systematic reviews and meta‐analyses with a total of 27 findings are identified. The health effect of consuming spicy food and chili peppers is unclear. Furthermore, the characteristics and context of different world regions and populations should be carefully considered. Direct correlations exist in esophageal cancer, gastric cancer, and gallbladder cancer. However, negative connections are reported in metabolism, mortality, and cardiovascular disease. Dose–response analysis reveals a significant nonlinear relationship between gastric cancer risk and capsaicin intake. The consumption of spicy foods and chili peppers is typically safe. However, high‐quality proof is available to confirm this conclusion.

The transcription factor c-Myc and two cullin family members CUL4A/4B function as oncogenes in colorectal cancer. Our recent publication reveals that c-Myc specifically activates the expression of CUL4A/4B through binding to their promoters. However, the underlying mechanism of how c-Myc actions in this process is still unknown. Using mass spectrometry and immunoprecipitation assays, we identified c-Myc formed a transcriptional complex with its partner Max (Myc-associated factor X), a histone acetyltransferase p300 and a coactivator associated arginine methyltransferase 1 (CARM1) in the present study. Knockdown or overexpression of the components of CARM1-p300-c-Myc-Max (CPCM) complex resulted in a decrease or increase of CUL4A/4B levels, respectively. Individual knockdown or inhibition of CPCM components decreased cell proliferation, colony formation, and cell invasion. Biochemically, knockdown or inhibition of CPCM components decreased their occupancies on the promoters of CUL4A/4B and resulted in their downregulation. Importantly, inhibition of CPCM components also caused a decrease of CRL4 E3 ligase activities and eventually led to an accumulation of ST7 (suppression of tumorigenicity 7), the specific substrate of CRL4 E3 ligases in colorectal cancer. Moreover, the in vivo tumor formation results indicated that knockdown or inhibition of CPCM components significantly decreased the tumor volumes. Together, our results suggest that the CPCM complex mediates explicitly the expression of CUL4A/4B, and thus affects the stability of CRL4 E3 ligases and the ubiquitination of ST7. These results provide more options by targeting the CPCM components to inhibit tumor growth in the therapy of colorectal cancer.

The aims of this study were to determine (1) the agreement in Epworth Sleepiness Scale (ESS) evaluated by patients and their close relatives (CRs), and (2) the correlation of objective sleepiness as measured by multiple sleep latency test (MSLT) with self-evaluated and close relative-evaluated ESS. A total of 85 consecutive patients with obstructive sleep apnea (OSA) (70 males, age 46.7 ± 12.9 years old) with an apnea-hypopnea index (AHI) > 5 events per hour (mean 38.9 ± 26.8/h) were recruited into this study. All participants underwent an overnight polysomnographic assessment (PSG), MSLT, and ESS rated by both patients and their CRs. Mean sleep latency < 8 min on MSLT was considered objective daytime sleepiness. Self-evaluated global ESS score (ESSG) was closely correlated with evaluation by CRs (r = 0.79, p < 0.001); the mean ESSG score evaluated by patients did not significantly differ from that evaluated by CRs (p > 0.05). However, Bland- Altman plot showed individual differences between self-evaluated and CR-evaluated ESS scores, with a 95%CI of -9.3 to 7.0. The mean sleep latency on MSLT was significantly associated with CR-evaluated ESSG (r = -0.23, p < 0.05); significance of association with self-evaluated ESSG was marginal (r = -0.21, p = 0.05). CR-evaluated ESS has a good correlation but also significant individual disagreement with self-evaluated ESS in Chinese patients with OSA. CR-evaluated ESS performs as well as, if not better than, self-evaluated ESS in this population when referring to MSLT.

Cullin 4A and 4B (CUL4A and 4B) function as oncogenes in colorectal cancer (CRC) cells. Both of them conservatively associate with DNA damage-binding protein 1 (DDB1) and DDB1-CUL4-associated factor 4 (DCAF4) to form Cullin-RING E3 ligases known as CRL4^DCAF4, which specifically ubiquitinate and degrade tumor suppressor ST7 (suppression of tumorigenicity 7). Knockdown either CUL4A/4B or DDB1 significantly inhibits tumor cell growth in vitro and in vivo. Thus, targeting these CRL4^DCAF4 components and their interactions may be an effective strategy for the therapy of CRC. In this study, we developed an in vitro AlphaScreen assay to identify small molecules targeting the CUL4A-DDB1 interaction. We obtained a compound NSC1892, which strongly disrupted the CUL4A-DDB1 interaction (IC₅₀ = 1.8 μM). Oncogenic phenotype analyses indicated that NSC1892 showed significant cytotoxicity to decrease cell proliferation, colony formation and invasion in CRC cells. Biochemical analyses demonstrated that NSC1892 treatment did not change CUL4A and CUL4B protein levels, but caused the degradation of DDB1, thereby leading to the impaired assembly of CRL4^DCAF4 E3 ligases and resulting in the accumulation of ST7. The administration of NSC1892 in mice also significantly inhibited tumor growth through degrading DDB1 and accumulating ST7. Interestingly, NSC1892 also showed promising cytotoxicity to decrease the growth of other CUL4A- or CUL4B-overexpressing tumor cells such as SKOV3 ovarian cells and Saos2 osteosarcoma cells. Our results provide a new avenue for the development of a therapeutic compound targeting tumors through disrupting the CUL4-DDB1 interaction.