OBJECTIVE:To investigate the intervention effects of (E)-4-[2-(4-chlorophenoxy)-2-methylpropanoyloxy]-3-me-thoxyphenyl acrylic acid (AZ) on fat accumulation in human hepatoma HepG2 cells. METHODS:Oleic acid was used to induce fat accumulation in HepG2 cells in logarithmic phase for establishing models of fat accumulation,which were divided into a model group,a positive control group(100 μg/ml simvastatin),and the groups of 15.63,31.25,62.5,125,250,500 and 1 000 μg/ml AZ,and a normal control group was set up. MTT method was used to detect the survival rates of all groups of cells,kit was per-formed to determine the contents of triglyceride (TG) in all groups of cells and calculate the clearance rates,and oil red O stain was conducted to observe the lipid droplet morphology of all groups of cells. RESULTS:Compared to the normal control group, the model group and the groups of 15.63-125 μg/ml AZ demonstrated no obviously different survival rate of cells,and the groups of 250-1 000 μg/ml AZ had lower survival rate of cells. There was statistically significance (P<0.05). The contents of TG in the cells of the model group were higher than those in the cells of the normal control group. The positive control group and the groups of 62.5 and 125 μg/ml AZ had lower contents of TG in the cells compared to the model group,showing a TG clearance rate of (28.58 ± 0.15)%,(14.51 ± 0.09)% and (29.72 ± 0.16)% respectively. There was statistically significance (P<0.01 or P<0.05). There were much more lipid droplets in the cells of the model group than in those of the normal control group. The lipid droplets in AZ groups gradually became less in quantity and smaller with the increasing in drug concentration. CONCLUSIONS:AZ has inter-vention effect on fat accumulation in HepG2 cells.

Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation of CRC cell proliferation, migration and survival. Inhibition of SGK1 represents a novel strategy for the treatment of CRC.
Animals ; Apoptosis ; Cause of Death ; Cell Proliferation ; Colon ; Colorectal Neoplasms* ; Fluorouracil ; Heterografts ; Humans ; In Vitro Techniques ; Mice ; Repression, Psychology ; RNA, Small Interfering

Objective:To investigate the relationship between serum Mir-137 and Mir-140 levels and clinicopathological features of breast cancer patients and recurrence and metastasis after postoperative chemotherapy with adriamycin + cyclophosphamide + docetaxel (ACT) .Methods:Female breast cancer patients who received chemotherapy of ACT regimen after modified radical mastectomy or breast-conserving radical mastectomy in Tongcheng People’s Hospital from Jan. 2017 to Apr. 2019 were included as research objects, and 60 healthy subjects who underwent physical examination in our hospital during the same period were included as healthy control group. Two ml of fasting peripheral venous blood was extracted from all patients before surgery and 1 week after the end of chemotherapy, and the relative expression levels of Mir-137 and Mir-140 in serum were determined by quantitative real-time polymerase linked reaction. Clinicopathological data were collected, including age, menopausal status, pathological type, TNM stage, estrogen receptor (ER) status, progesterone receptor, PR and human epidermal growth factor receptor-2 (HER2) status. All breast cancer patients were followed up for 3 years after surgery, and postoperative recurrence, distant metastasis and death time were recorded according to medical records and follow-up results.Results:The relative expression of Mir-137 in breast cancer patients was 0.89±0.15, significantly lower than that in healthy controls (1.34±0.21) ( t=4.985, P<0.001) . The relative expression of Mir-140 in breast cancer patients was 0.83±0.14, significantly lower than that in healthy controls (1.18±0.17) ( t=4.245, P<0.001) . Serum Mir-137 level was correlated with TNM stage, ER status and HER2 status in breast cancer patients ( t=2.56, 2.06, 2.24, P=0.003, 0.007, 0.004) , and serum Mir-140 level was correlated with TNM stage and HER2 status in breast cancer patients ( t=1.954, 2.114, P=0.008, 0.006) . After chemotherapy, the relative expression levels of serum Mir-137 and serum Mir-140 in breast cancer patients were 1.05±0.16 and 0.97±0.18, respectively, significantly higher than those before surgery ( t=2.689 and 3.051, P=0.004 and 0.002, respectively) . A total of 17 patients developed recurrence or distant metastasis within 3 years, and the 3-year progression-free survival rate was 71.67% (43/60) . The mir-137 level of patients with recurrent metastasis was 0.74±0.14, significantly lower than that of patients without recurrent metastasis (0.94±0.13) , the difference was statistically significant ( t=4.149, P<0.001) . The mir-140 level of patients with recurrent metastasis was 0.73±0.10, which was significantly lower than that of patients without recurrent metastasis (0.87±0.13) , the difference was statistically significant ( t=3.634, P<0.001) . ROC curve analysis showed that the sensitivity and specificity of serum Mir-137 expression level in predicting recurrence and metastasis of breast cancer patients were 82.4% and 79.1%, respectively. The sensitivity and specificity of serum Mir-140 expression level in predicting recurrence and metastasis of breast cancer patients were 82.4% and 69.8%, respectively. Kaplan-meier survival curve analysis showed that the 3-year progression-free survival rate of patients with low Mir-137 level was significantly lower than that of patients with high Mir-137 level ( P=0.025) . There was no significant difference in 3-year progression-free survival between patients with low mir-140 level and those with high Mir-140 level ( P=0.282) . Conclusion:Serum Mir-137 and Mir-140 levels are related to clinicopathological features and the efficacy of ACT chemotherapy after operation, which can be used as indicators to evaluate the disease and prognosis.

Myocardial fibrosis is a common pathological manifestation of various heart diseases,with hidden onset and the possibility of evolving into irreversible heart failure.Currently,there is still insufficient diagnosis and treatment of myocardial fibrosis.Traditional Chinese medicine can regulate myocardial fibrosis at multiple levels,targets,and pathways,and has significant advantages in treating myocardial fibrosis.Its underlying mechanisms are worth further exploration.The theory of"yang generating qi,yin constituting the body"in Huangdi Neijing embodies the meaning of yin and yang,containing a profound outlook on life and disease.Pathological changes in the initial,progressive,and final stages of myocardial fibrosis conform to the yin-yang theory of"yang generating qi,yin constituting the body".Insufficient yang generating qi and excessive yin constituting the body constitutes the core pathogenesis of myocardial fibrosis.This article proposes a treatment approach for myocardial fibrosis by tonifying yang and abating yin.The treatment of warming yang,unblocking yang,removing blood stasis,resolving phlegm,detoxifying,and promoting diuresis is applied to broaden the clinical treatment approach for myocardial fibrosis.