Long-term straw return improves cooked indica rice texture by altering starch structural, physicochemical properties in South China.

Straw return can improve rice eating quality by modifying starch formation from long-term field trials, whereas the relevant mechanisms are still unknown. A long-term field experiment, including straw removal (CK), straw burning return (SBR), and straw return (SR) was conducted to investigate the starch structure, physicochemical properties, and cooked rice textures of indica early- and late-rice. Compared with CK, SBR and SR enhanced relative crystallinity, amylopectin long chains in both rice seasons, and gelatinization temperatures in late rice. Compared to SBR, SR decreased protein content and amylopectin short chains but increased starch branching degree, breakdown, and stickiness, ultimately contributing to improved starch thermal and pasting properties. Meanwhile, SR decreased hardness, cohesiveness, and chewiness, resulting in cooked texture meliorated, which was mainly attributed to amylopectin chain length and starch granule size. The results suggest that SR increased cooked texture of indica rice by altering starch structural and physicochemical properties.

Knockdown of S100A11 expression suppresses ovarian cancer cell growth and invasion.

As a member of the S100 protein family, S100A11 expression is often upregulated in human cancer tissues. Numerous studies have demonstrated that S100A11 plays an important role in the progression of cancer. However, the function of S100A11 in ovarian cancer remains elusive. In the present study, the expression levels of S100A11 were found to be significantly increased in ovarian cancer cells. Subsequently, the expression of S100A11 in ovarian cancer HO8910 cells was knocked down using short hairpin (sh)RNA in order to investigate the biological effects of S100A11 on the progression of the disease. The results demonstrated that knockdown of S100A11 by shRNA inhibited the proliferation, anchorage-independent growth, invasion and migration of HO8910 cells. In addition, knockdown of S100A11 increased the expression of E-cadherin and decreased the expression of Snail in HO8910 cells. Collectively, these results indicated that S100A11 was able to promote the growth, invasion and migration of ovarian cancer cells. Therefore, S100A11 may serve as a potential molecular target for the diagnosis and treatment of ovarian cancer.

Inhibition of Akt signaling by SN-38 induces apoptosis in cervical cancer.

Cervical cancer still remains a major health problem in women worldwide. Inhibitors of topoisomerase I have proven to be among the most promising new classes of anti-neoplastic agents introducing into the clinic in recent years. CPT-11 is one of the most widely used Camptothecin analogues and is converted to form the active metabolite SN-38. The study tried to explore the in vitro mechanisms of apoptosis induced by SN-38 in cervical cancer cell lines HeLa and SiHa. The results demonstrated here that SN-38 inhibited cell proliferation in a time- and dose-dependant manner. Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt. Transfection of the full-length Akt cDNA into HeLa and SiHa cells resulted in the reduction of apoptosis induced by SN-38, and Akt kinase activity regulated the p53 pathway, indicating that inhibition of the Akt pathway played an important role in exhibition of SN-38-mediated cytotoxic effect. Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.

Apoptosis of HeLa cells induced by cisplatin and its mechanism.

To study the apoptosis induced by cisplatin in cervical cancer cell line HeLa and its mechanism, cell growth inhibition of cisplatin on HeLa cells was analyzed by MTT assay. Cell apoptosis was examined by cytometry and Hoechst33258 staining after treatment with cisplatin. The effects of cisplatin on transcription of E6 were analyzed by RT-PCR. The protein expressions of E6, p53, p21, Bax and Bcl-2 were studied by Western blotting. Cisplatin inhibited proliferation in a time-and dose-dependant manner. Cytometically, sub-G(1) peak showed higher apoptosis rates in the experimental group than those in the control. Hoechst33258staining exhibited apoptosis induced by cisplatin. RT-PCR revealed that cisplatin decreased transcription of E6. Western blotting showed that cisplatin decreased protein expression of E6 and increased protein expression of p53, p21 and Bax. It had no effect on protein expression of Bcl-2. It is concluded that cisplatin can induce apoptosis in HeLa cells by suppressing HPV E6 and thereby restoring the function of p53.

[Relationship between VEGF-C expression and nasopharyngeal carcinoma proliferation and metastasis].

OBJECTIVE: To detect the expression of VEGF-C in nasopharyngeal carcinoma (NPC) and explore its relationship with proliferation and metastasis of NPC. METHODS: Biopsy specimens of 62 NPC patients were divided into 2 equal portions, one for immunohistochemical staining with VEGF-C polyclonal antibody by streptavidin peroxidase method, another for flow cytometry with Ki67 antibody to analyze the proliferation of tumors. The patients were followed up periodically, and then their 3-year survival and the cause of death were statistically analyzed. RESULTS: Of the 62 patients, the percentage of VEGF-C positive cells in the tumors ranged from 0 - 82%, 17 (27.4%) were negative, 13 (21.0%) weak positive, 18 (29.0%) moderate positive and 14 (22.6%) strong positive. Ki67 positive tumor cells ranged from 0 - 52%, 40 cases (64.5%) showed low expression which include 15 cases of negative, 22 (35.5%) showed high expression. There was a direct relationship between the expression of VEGF-C and Ki67 (r = 0.323, P < 0.05). The 3-year survival rate of 62 patients was 66.1%. The expression of VEGF-C in the patients with positive lymph node was much higher than that with negative lymph node (P < 0.01). Among the 8 patients with distant metastasis, their VEGF-C expression was strong positive while among the 21 disease free survival patients, their VEGF-C expression was (-) or (+) account for 80.9%. An inverse correlation was found between the VEGF-C expression and prognosis of NPC patients, but the difference has no statistical significance (r = -0.219, P > 0.05). CONCLUSION: High expression of VEGF-C is related with proliferation and metastasis of NPC cells. It is not an independent prognostic factor, but a predictive marker of disease-free survival of NPC patients.

[Inhibitory effects of tetraethylammonium on proliferation and voltage-gated potassium channels in human cervical carcinoma cell line SiHa].

BACKGROUND & OBJECTIVE: Various potassium channels are known to be involved in proliferation of many malignant cell lines. This study was to explore the role of voltage-gated potassium channels in proliferation of human cervical carcinoma cells through observing the effects of tetraethylammonium (TEA) on proliferation and outward potassium currents in human cervical carcinoma cell line SiHa. METHODS: SiHa cells were treated with TEA. The effect of TEA on proliferation of SiHa cells was assessed by MTT assay. Cell apoptosis and cell cycle were detected by flow cytometry with Hoechst 33258 staining. The outward potassium currents were recorded by patch clamp technique. RESULTS: TEA inhibited the proliferation of SiHa cells in dose-and time-dependent manners, and induced cell apoptosis. The cell cycle was arrested at G0/G1 phase after treatment with TEA. Exposure of SiHa cells to 10 mmol/L TEA reduced the peak outward potassium currents significantly from (260+/-12) pA to (58+/-6) pA (P<0.01). CONCLUSIONS: Voltage-gated potassium channels play an important role in regulating proliferation of cervical carcinoma SiHa cells. Blocking voltage-gated potassium channels could inhibit proliferation of SiHa cells.