scholarly journals Anticancer Activity of Binary Toxins from Lysinibacillus sphaericus IAB872 against Human Lung Cancer Cell Line A549

2014 ◽  
Vol 9 (1) ◽  
pp. 1934578X1400900
Author(s):  
Wenjuan Luo ◽  
Cuicui Liu ◽  
Ruijuan Zhang ◽  
Jianwei He ◽  
Bei Han
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Cell Apoptosis ◽  
Human Lung ◽  
Immunocytochemical Staining ◽  
Lysinibacillus Sphaericus ◽  
Proliferative Effect

The inhibitory effect of binary toxic (Bin) protein produced by Lysinibacillus sphaericus IAB872 on cell proliferation of human lung, liver, stomach and cervical tumor cell lines was assessed using MTT assay. The effect of Bin protein on A549 cell proliferation, apoptosis, cell cycle, migration and invasion were examined by MTT assay, Western blotting, Immunocytochemical staining, flow cytometry assay and wound-healing assay. Results showed that Bin protein inhibits proliferation of a range of human cancer cells in vitro. The anti-proliferative effect of Bin is associated with cell apoptosis as a result of an increased ratio of cellular Bax/bcl-2, up-regulated CyclinB1and down-regulated Cdc25c expression, and its anti-proliferative action was associated with cell cycle arrest in the G2/M-phase. Bin protein could promote apoptosis and inhibit motility and invasion of A549 cancer cells. The anti-proliferative effect of Bin protein was associated with the induction of apoptotic cell death and cell cycle disruption. These results show that Bin protein has the potential to be developed as a chemotherapeutic agent by induction of human tumor cell apoptosis.

scholarly journals Anticancer effect of 7-hydroxycoumarin in cisplatin-resistant ovarian cancer cell is mediated via apoptosis induction, caspase activation and cell cycle arrest at G2M phase

2022 ◽  
Vol 20 (2) ◽  
pp. 281-286
Author(s):  
Hongmei Wang ◽  
Yina Wang
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Anticancer Effect ◽  
Cycle Arrest

Purpose: To investigate the anticancer effects of 7-hydroxycoumarin against cisplatin-resistant ovarian cancer cell line, and the underlying mechanism(s). Methods: Cell proliferation was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The 4’,6-diamidino-2-phenylindole (DAPI) and acridine orange/ethidium bromide (AO/EB) dual staining methods were used for measuring cell apoptosis in terms of DNA damage. Flow cytometry was used for analysis of mitosis of cancer cells, while protein expression levels were assayed with western blotting. Results: The 7-hydroxycoumarin preferentially inhibited the proliferation of the ovarian cancer cells, but had significantly less prominent effects on normal cells (p < 0.05). The decrease in cell proliferation was due to induction of cell apoptosis via caspase-linked apoptotic pathway. Treatment with 7- hdoxycoumarin further led to the arrest of cancer cell cycle at G2/M stage (p < 0.05) via down-regulation of the expressions of regulatory proteins that promote mitotic entry. Conclusion: 7-Hydroxycoumarin exerts significant anticancer effect against cisplatin-resistant ovarian cancer cells via decrease in cell proliferation, induction of apoptosis and mitotic cell cycle arrest. Thus, the compound could emerge as a vital lead molecule in the treatment of cisplatin-resistant type of human ovarian cancer.

Effect of Yes Associated Protein 1 Silence on Proliferation and Apoptosis of Bladder Cancer Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 857-863
Author(s):  
Gaoliang Wu ◽  
Chao Hao ◽  
Xueliang Qi ◽  
Jianqiang Nie
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Direct Role ◽  
Cycle Arrest ◽  
Proliferation And Apoptosis ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Yes Associated Protein 1 (YAP) can act as either an oncoprotein or a tumor suppressor in different cellular contexts. However, the reports about the direct role of YAP silence in bladder cancer cells are rare. We designed loss-off-function experiments to investigate the effect of YAP knockdown on bladder cancer cell proliferation, cell cycle and cell apoptosis. We examined YAP expression in human bladder cancer and paracancerous tissues using RT-qPCR, western blot and immunohisto-chemistry. YAP short hairpin RNA (shRNA) was successfully constructed and transfected into T24 cells to knockdown YAP. Cell proliferation, cell cycle and cell apoptosis were analyzed by CCK-8 and flow cytometry. We found the expression levels of YAP mRNA and protein were significantly increased in the bladder cancer tissues when compared with that in the paracancerous tissues. shRNA YAP inhibited cell proliferation, induced cell cycle arrest at G1 phase, and induced cell apoptosis. In conclusion, our findings provided the first evidence that YAP knockdown could inhibit cell proliferation and induce cell apoptosis of bladder cancer cells. YAP inhibition may be beneficial in the treatment of bladder cancer.

Beta-Caryophyllene Suppresses Ovarian Cancer Proliferation by Inducing Cell Cycle Arrest and Apoptosis

2020 ◽  
Vol 20 (13) ◽  
pp. 1530-1537 ◽  
Author(s):  
Santhosh Arul ◽  
Harinee Rajagopalan ◽  
Jivitesh Ravi ◽  
Haripriya Dayalan
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Parp Cleavage ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Proliferative Effect ◽  
Cycle Arrest

Background: Ovarian cancer is the fifth most common cause of cancer deaths among women with lesser prognostics. Current treatment options are chemotherapy with platinum and taxane based chemotherapy. β-Caryophyllene (BCP) an essential oil found in many plant species is known to possess an anti-proliferative effect. Objective: We aimed to investigate the antiproliferative, cytotoxic, and apoptotic role of BCP against ovarian cancer cells PA-1 and OAW 42. Methods: The antiproliferative effect of BCP was determined by MTT assay and cell viability by trypan blue exclusion assay. Cell cycle and live/dead cell analyses were performed by flow cytometry to determine cell cycle distribution and apoptosis, respectively. Results: Results of MTT assay proved the anti-proliferative effect of BCP in a dose and time-dependent manner in ovarian cancer cells. Cell cycle analysis showed that BCP induced S Phase arrest in OAW 42 cells. Results of apoptosis assay confirmed the apoptosis inducing potential of BCP in ovarian cancer cells. The apoptosis is mediated by caspase-3 activation and PARP cleavage. Conclusion: The results of our present study prove that BCP exerts its action partly by inducing cell cycle arrest and apoptosis in ovarian cancer. We conclude that BCP is a potential anti-cancer agent.

scholarly journals Long Noncoding RNA Urothelial Carcinoma-Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144

2018 ◽  
Vol 26 (4) ◽  
pp. 537-546 ◽  
Author(s):  
Dagang Li ◽  
Huizong Li ◽  
Yuping Yang ◽  
Le Kang
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Viability ◽  
Cancer Cells ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Human Lung ◽  
Proliferation And Metastasis

Long noncoding RNA urothelial carcinoma-associated 1 (lncRNA UCA1) has gained more attention in recent years due to its oncogenic roles in various cancers. MicroRNA-144 (miR-144) participates in the regulation of the growth of many cancer cells. This study investigated the interaction between lncRNA UCA1 and miR-144 in lung cancer cells. The potential downstream protein of miR-144 was also assessed. Our results found that lncRNA UCA1 was highly expressed in human lung cancer A549, H517, H4006, H1299, and H1650 cells compared to normal embryonic lung WI-38 and HEL-1 cells. Knockdown of lncRNA UCA1 significantly inhibited lung cancer A549 cell viability, migration, invasion, and cell cycle progression, but promoted cell apoptosis. Besides, we found that lncRNA UCA1 was bound to miR-144. miR-144 participated in the regulation effects of lncRNA UCA1 on A549 cell viability, migration, invasion, cell cycle transition, and cell apoptosis. In addition, Pre-B-cell leukemia homeobox 3 (PBX3) was found to be a direct target gene of miR-144. Overexpression of PBX3 promoted A549 cell proliferation and metastasis. Suppression of PBX3 had an opposite effect.

scholarly journals Polarity Protein Par3 Sensitizes Breast Cancer to Paclitaxel by Promoting Cell Cycle Arrest.

2021 ◽  
Author(s):  
She Chen ◽  
Yannan Zhao ◽  
Huitong Peng ◽  
Limiao Liang ◽  
Yi Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Brdu Incorporation ◽  
Individual Treatment ◽  
Breast Cancer Patients ◽  
Kaplan Meier

Abstract Purpose Paclitaxel, belongs to tubulin-binding agents (TBAs), showed a great efficacy against breast cancer via stabilizing microtubules. Drug resistance limits its clinical application. Here we aimed to explore a role of Polarity protein Par3 in improving paclitaxel effectiveness.Methods Breast cancer specimens from 45 patients were collected to study the relationship between Par3 expression and paclitaxel efficacy. The Kaplan–Meier method was used for survival analysis. Cell viability was measured in breast cancer cells (SK-BR-3 and T-47D) with Par3 over-expression or knockdown. The flow cytometry assays were performed to measure cell apoptosis and cell cycle. BrdU incorporation assay and Hoechst 33258 staining were performed to measure cell proliferation and cell apoptosis, respectively. Immunofluorescence was used to detect microtubule structures. Results Par3 expression is associated with good response of paclitaxel in breast cancer patients. Consistently, Par3 overexpression significantly sensitizes breast cancer cells to paclitaxel by promoting cell apoptosis and reducing cell proliferation. In Par3 overexpressing cells upon paclitaxel treatment, we observed intensified cell cycle arrests at metaphase. Further exploration showed that Par3 overexpression stabilizes microtubules of breast cancer cells in response to paclitaxel, and resists to microtubules instability induced by nocodazole, a microtubule-depolymerizing agent. Conclusion Par3 facilitates polymeric forms of tubulin and stabilizes microtubule structure, which aggravates paclitaxel-induced delay at the metaphase-anaphase transition, leading to proliferation inhibition and apoptosis of breast cancer cells. Par3 has a potential role in sensitizing breast cancer cells to paclitaxel, which may provide a more precise assessment of individual treatment and novel therapeutic targets.

scholarly journals The Investigation of the Effects of Tamoxifen and Vitamin D Combination on the Expression of P53, Bcl-2 and Bax and Cell Cycle in Mcf-7 Cell Line

Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1527
Author(s):  
Derya Yetkin ◽  
Ebru Ballı ◽  
Gülsen Bayrak ◽  
Deniz Kibar ◽  
Merve Türkegün
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Vitamin D ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Line ◽  
G1 Phase ◽  
Breast Cancer Patients ◽  
Proliferative Effect ◽  
Cell Arrest

Breast cancer is the leading type of cancer in women. The majority of cells in the diagnosis of breast cancer are estrogen receptor alpha (ER α) positive and the growth of these tumors is due to estrogen. Tamoxifen is used as a supportive treatment method in breast cancer patients. Vitamin D is a group of sterols with hormone-like functions. Vitamin D is known to have anti-proliferative effect and is known to induce cell arrest and apoptosis in the G0/G1 phase in the cell cycle. This study aims to investigate the potential anti-carcinogenic effect of different concentrations of Tamoxifen and vitamin D, which are thought to have anti-proliferative effect on breast cancer cell line. In our study, combination of different concentrations of Tamoxifen and vitamin D was evaluated. As a result of the data obtained, cell cycle was studied in FACS ARIA III device. In addition, the expression of p53, BcL-2 and Bax proteins was examined in qRT PCR. In our study, low concentrations of Tamoxifen and vitamin D increased proliferation in cancer cells. An effective concentration was found for Tamoxifen. Vitamin D alone did not reduce cell proliferation but decreased cell proliferation with combination. As a result, it was found that therapies using these two agents separately decreased the proliferation of cancer cells and induced cell arrest in the G0/G1 phase in the cell cycle and changed the expressions of p53, BcL-2 and Bax proteins.

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