Caveolin,a membrane protein of 21-24 k,is the main structural component of caveolae,it plays quite a diverse functional role in maintaining vital activities of cells like endocytosis,cholesterol transport,cell membrane composition,and transduction of transmembrane signal to some virus involved in the processes of virus infection.Caveolin-1 also is a key regulator of multiple steps of oncogenesis and tumor development.Caveolin-1 can also serve as a negative regulator in proliferation,apoptosis,invasion and metastasis in varieties of cancer cells.There are some conflicting roles in different tumors,this review summarized the recent advances in the function of caveolin in cancers.

Focal adhesion kinase(FAK),the non-receptor tyrosine kinase,has been implicated in regulating a number of fundamental biological signal transudation pathways that control cell proliferation,survival,adhesion,motility.Many researches have reported that FAK highly expressed in many cancers and involved in the process of cancer development,such as initial,progress,metastasis,multi-drug resistance of cancer.FAK has been the hotpot in cancer research,and it will be a new target in cancer therapy.

To identify the best inducing condition, we studied the expression of membrane protein HSP70 and mRNA of H22 cell at various temperature. Using MTT,RT-PCR, immunofluorescence and FCM techniques, we observed H22 cell survival rate, the expression of HSP70 mRNA and membrane HSP70. No effects of H22 cell survival rate under 42 ~ 43℃ was observed, but cell survival rate declined with increasing stress time at 44 ~ 45 ℃; the level of HSP70 mRNA decreased initially (0.5~4.0) hours but gradually resumed and increased from 8 to 12 hours at 42℃. Membrane HSP70 expressing cells were significently higher in heat shock treatment group than in a control group ( P

OBJECTIVE： To synthetize the synthesis of mitoxantrone and evaluate its quality. METHODS： Crude product of mitoxantrone was prepared by slow oxidation of 1，4，5，8-tetrahydro-anthraquinone with N-（2-hydroxyethyl） ethylenediamine in water bath at 50 ℃ for 2 h under argon protection and in dry air for 4 h. The crude product was crystallized by ethanol-n-hexane  （4 ∶ 1，V/V） mixture solution， which was cooled overnight and then washed by ethanol-n-hexane mixture for many times. The melting range， pH value of solution， ultraviolet-visible absorption spectrum， infrared structural characteristics， drying weight loss （water loss rate） and critical relative humidity （CRH） of the purified products （4 batches） were investigated. HPLC method was used to determine the contents of mitoxantrone. RESULTS： The mitoxantrone was prepared successfully， and synthetic yield of mitoxantrone was 34.3％； the melting point ranged from 159.1-163.6 ℃. The aqueous solution was alkaline （pH 7.63-9.54）； there was a maximum ultraviolet absorption peak at 235-245 nm； there was a maximum absorption peak of visible light at 590-600 nm； the infrared characteristics were consistent with those described of mitoxantrone in the 2015 edition of the Infrared Spectrum Collection of Drugs； water loss rate were －0.83％-2.36％； CRH value was 54.7％， and the average content of the product was 78.1％（n＝4） by HPLC method. CONCLUSIONS： The mitoxantrone is synthesized under mild， non-toxic and harmless experiment conditions. The synthesis step is simple， the cost is low and the yield is high. The quality of products meets the quality requirements.

ObjectiveTo explore the therapeutic effect and mechanism of intermittent theta burst transcranial magnetic stimulation (iTBS) on non-fluent aphasia after stroke. MethodsFrom August, 2021 to August, 2022, 50 patients with non-fluent aphasia after stroke in the First People's Hospital of Lianyungang were randomly divided into sham stimulation group (n = 25) and iTBS group (n = 25). Both groups accepted speach training. iTBS group accepted iTBS, and the sham stimulation group received sham iTBS, for four weeks. The serum brain-derived neurotrophic factor (BDNF) was measured, and they were assessed by China Rehabilitation Research Center Standard Aphasia Examination (CRRCAE) and Boston Diagnostic Aphasia Examination before and after treatment. ResultsTwo cases in the sham stimulation group and three cases in iTBS group dropped down. The BDNF level, and listen and understand, repeat, name, read aloud, and total score of CRRCAE improved in two groups after treatment (|t| > 5.012, P < 0.001); and they were better in iTBS group than in the sham stimulation group (|t| > 3.968, P < 0.001). The total effective rate was more in iTBS group than in the sham stimulation group (χ² = 8.835, P < 0.05). ConclusioniTBS can improve speech function in patients with non-fluent aphasia after stroke, which may associate with the promotion of BDNF.

In this study, we used a rat model of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) to investigate the role and mechanism of angiotensin (Ang)-(1-7) in regulating pulmonary artery diastolic function. Three weeks after subcutaneous injection of MCT or normal saline, the right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of rats were detected using a right heart catheter. Vascular endothelium-dependent relaxation was evaluated by acetylcholine (ACh)-induced vasodilation. The relaxation function of vascular smooth muscle was evaluated by sodium nitroprusside (SNP)-induced vasodilation. Human pulmonary artery endothelial cells (HPAECs) were incubated with Ang-(1-7) to measure nitric oxide (NO) release levels. The results showed that compared with control rats, RVSP and RVHI were significantly increased in the MCT-PAH rats, and both ACh or SNP-induced vasodilation were worsened. Incubation of pulmonary artery of MCT-PAH rats with Ang-(1-7) (1 × 10^-9-1 × 10^-4 mol/L) caused significant vaso-relaxation. Pre-incubation of Ang-(1-7) in the pulmonary artery of MCT-PAH rats significantly improved ACh-induced endothelium-dependent relaxation, but had no significant effect on SNP-induced endothelium-independent relaxation. In addition, Ang-(1-7) treatment significantly increased NO levels in HPAECs. The Mas receptor antagonist A-779 inhibited the effects of Ang-(1-7) on endothelium-dependent relaxation and NO release from endothelial cells. The above results demonstrate that Ang-(1-7) promotes the release of NO from endothelial cells by activating Mas receptor, thereby improving the endothelium-dependent relaxation function of PAH pulmonary arteries.
Rats ; Humans ; Animals ; Vasodilation ; Pulmonary Arterial Hypertension ; Monocrotaline/toxicity* ; Rats, Sprague-Dawley ; Hypertension, Pulmonary/chemically induced* ; Endothelial Cells ; Pulmonary Artery ; Endothelium ; Acetylcholine/pharmacology* ; Nitroprusside/pharmacology*

OBJECTIVETo investigate the effect of 17-allylamino-demethoxygeldanamycin (17AAG) on the proliferative and invasive ability of gastric cancer cells and associated mechanism.

METHODSThe proliferative ability was tested by MTT method and the cell cycle was detected by flow cytometry(FCM) when 17AAG was used to treat gastric cancer cell SGC7901. Apoptosis was detected by FCM and PI-Annexin V double staining. The invasive ability was tested by transwell method. Expression of HSP90, HSP70, c-met and AKT was detected by Western blot.

RESULTSThe growth of SGC7901 cells was inhibited after the administration of 17AAG, and the inhibitation was dose- and time-dependent. The cell cycle was blocked at the G0/G1 phase. The apoptotic ratio in 17AAG group was much higher than that in blank group and DMSO group (P<0.01). The cellular invasive ability decreased significantly (P<0.01). The expression of HSP70 was elevated by 17AAG, and the expression of c-met and AKT was down-regulated, but no change of HSP90 was observed.

CONCLUSION17AAG can inhibit the proliferative and invasive ability of SGC7901 cells, and induces apoptosis through down-regulating the expression of HSP90 client proteins instead of the target HSP90 itself.

Apoptosis ; Benzoquinones ; pharmacology ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; HSP70 Heat-Shock Proteins ; HSP90 Heat-Shock Proteins ; Humans ; Lactams, Macrocyclic ; pharmacology ; Neoplasm Invasiveness ; Stomach Neoplasms ; pathology

Objective To investigate the effect of 17-allylamino-demethoxygeldanamycin (17AAG) on the proliferative and invasive ability of gastric cancer cells and associated mechanism. Methods The proliferative ability was tested by MTT method and the cell cycle was detected by flow cytometry (FCM) when 17AAG was used to treat gastric cancer cell SGC7901. Apoptosis was detected by FCM and PI-Annexin V double staining. The invasive ability was tested by transwell method. Expression of HSP90, HSP70, c-met and AKT was detected by Western blot. Results The growth of SGC7901 cells was inhibited after the administration of 17AAG, and the inhibitation was dose- and time-dependent. The cell cycle was blocked at the G0/G1 phase. The apoptotic ratio in 17AAG group was much higher than that in blank group and DMSO group (P<0.01). The cellular invasive ability decreased significantly (P<0.01). The expression of HSP70 was elevated by 17AAG, and the expression of c-met and AKT was down-regulated, but no change of HSP90 was observed. Conclusion 17AAG can inhibit the proliferative and invasive ability of SGC7901 cells , and induces apoptosis through down-regulating the expression of HSP90 client proteins instead of the target HSP90 itself.

Objective To investigate the effect of 17-allylamino-demethoxygeldanamycin (17AAG) on the proliferative and invasive ability of gastric cancer cells and associated mechanism. Methods The proliferative ability was tested by MTT method and the cell cycle was detected by flow cytometry (FCM) when 17AAG was used to treat gastric cancer cell SGC7901. Apoptosis was detected by FCM and PI-Annexin V double staining. The invasive ability was tested by transwell method. Expression of HSP90, HSP70, c-met and AKT was detected by Western blot. Results The growth of SGC7901 cells was inhibited after the administration of 17AAG, and the inhibitation was dose- and time-dependent. The cell cycle was blocked at the G0/G1 phase. The apoptotic ratio in 17AAG group was much higher than that in blank group and DMSO group (P<0.01). The cellular invasive ability decreased significantly (P<0.01). The expression of HSP70 was elevated by 17AAG, and the expression of c-met and AKT was down-regulated, but no change of HSP90 was observed. Conclusion 17AAG can inhibit the proliferative and invasive ability of SGC7901 cells , and induces apoptosis through down-regulating the expression of HSP90 client proteins instead of the target HSP90 itself.

Objective To make a better understanding of the molecular mechanisms involved in recurrence and metastasis of the hepatocellular carcinoma (HCC), some invasion related oncogenes, and growth factors have been investigated. Methods The studies were seperately carried out, the results of which were summarized in this article with relation to tumor size and invasiveness of HCC.Results The aberration rates of p53 and CDKN2 in HCC were 45.9% and 36.4% respectively, which were higher in invasive HCC compared with non-invasive HCC. H-ras expression was positive in 29.3% of HCC, which was associated with recurrence and extrahepatic metastasis of HCC. Intralesional injection of H-ras antisense gene markedly inhibited the tumor growth and metastasis of HCC in nude mice. The positive rates of transforming growth factor (TGF)-alpha, epidermal growth factor receptor (EGFR) and c-erbB-2 were 45.7%, 47.1% and 92.3% respectively. The expression of EGFR was closely related to TGF-alpha, which was related to HCC recurrence. But no obvious difference of TGF-alpha or c-erbB-2 expression was found between HCC with and without recurrence, or with and without extrahepatic metastasis. Expression of nm23 / tissue inhibitor of metalloproteinase (TIMP)-2 was positively associated with the prognosis of HCC patients (Log-rank, P<0.001). The alterative rates of above-mentioned genes and growth factors in small HCC were slightly lower than that in large ones, but no significant difference was shown except the p53 mutation.Conclusions The p53/CDKN2 mutation, overexpression of H-ras/EGFR, were associated with the invasiveness and recurrence of HCC. H-ras antisense gene might be of potential implication in the control of HCC recurrence and metastasis. Expression of nm23/TIMP-2 was closely related to the prognosis of HCC patients. Biological characteristics remained critical points to the prognosis even in small HCC.