The krüppel-like factor5 (KLF5) regulates uterine endometrial cancer proliferation and migration

2019 ◽  
Vol 154 ◽  
pp. 101
Author(s):  
J. Kojima ◽  
K. Kubota ◽  
T. Moritake ◽  
T. Nagashima ◽  
H. Nishi
Keyword(s):  
Endometrial Cancer ◽  
Cancer Proliferation ◽  
Uterine Endometrial Cancer ◽  
And Migration ◽  
Proliferation And Migration

Rutin loaded liquid crystalline nanoparticles inhibit non-small cell lung cancer proliferation and migration in vitro

Life Sciences ◽  
2021 ◽  
Vol 276 ◽  
pp. 119436
Author(s):  
Keshav Raj Paudel ◽  
Ridhima Wadhwa ◽  
Xin Nee Tew ◽  
Natalie Jia Xin Lau ◽  
Thiagarajan Madheswaran ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Liquid Crystalline ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cancer Proliferation ◽  
Liquid Crystalline Nanoparticles ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals LPS-induced CXCR7 expression promotes gastric Cancer proliferation and migration via the TLR4/MD-2 pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Nan Li ◽  
Huanbai Xu ◽  
Yurong Ou ◽  
Zhenzhong Feng ◽  
Qiong Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Proliferation ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Human Umbilical Cord Mesenchymal Stem Cell-Derived Extracellular Vesicles Inhibit Endometrial Cancer Cell Proliferation and Migration through Delivery of Exogenous miR-302a

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xin Li ◽  
Li li Liu ◽  
Ju lei Yao ◽  
Kai Wang ◽  
Hao Ai
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cancer Cells ◽  
Umbilical Cord ◽  
Extracellular Vesicles ◽  
Target Cells ◽  
Human Umbilical Cord ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

MicroRNAs (miRNAs) are potential therapeutic targets in endometrial cancer, but the difficulties associated with their delivery to tumor target cells have hampered their applications. Human umbilical cord mesenchymal stem cells (hUCMSCs) have a well-recognized tumor-homing ability, emphasizing the capacity of tumor-targeted delivery of extracellular vesicles. hUCMSCs release extracellular vesicles rich in miRNAs, which play a vital role in intercellular communication. The purpose of this study was to verify a potential tumor suppressor microRNA, miR-302a, and engineered hUCMSC extracellular vesicles enriched with miR-302a for therapy of endometrial cancer. Here, we observed that miR-302a was significantly downregulated in endometrial cancer tissues when compared with adjacent tissues. Overexpression of miR-302a in endometrial cancer cells robustly suppressed cell proliferation and migration. Meanwhile, the proliferation and migration were significantly inhibited in endometrial cancer cells when cultured with miR-302a-loaded extracellular vesicles derived from hUCMSCs. Importantly, our data showed that engineered extracellular vesicles rich in miR-302 significantly inhibited the expression of cyclin D1 and suppressed AKT signaling pathway in endometrial cancer cells. These results suggested that exogenous miR-302a delivered by hUCMSC-derived extracellular vesicles has exciting potential as an effective anticancer therapy.

scholarly journals Lobaplatin Inhibits Prostate Cancer Proliferation and Migration Through Regulation of BCL2 and BAX

Dose-Response ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 155932581985098 ◽  
Author(s):  
Hongwen Cao ◽  
Yigeng Feng ◽  
Lei Chen ◽  
Chao Yu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cancer Proliferation ◽  
Expression Levels ◽  
And Migration ◽  
Proliferation And Migration

Lobaplatin is a diastereometric mixture of platinum (II) complexes, which contain a 1,2-bis (aminomethyl) cyclobutane stable ligand and lactic acid. Previous studies have showed that lobaplatin plays inhibiting roles in various types of tumors. However, the role of lobaplatin in prostate cancer remains unknown. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell proliferation was detected by cell colony formation assay. Cell migration and invasion were determined by transwell migration and invasion assay. Cell apoptosis was detected by flow cytometry. The messenger RNA and protein expression levels were detected by quantitative real-time polymerase chain reaction and Western blot. Lobaplatin treatment inhibits cell viability, cell proliferation, cell migration, and invasion, while promotes cell apoptosis of prostate cancer cell lines DU145 and PC3. Meanwhile, lobaplatin treatment regulates apoptosis by downregulation of BCL2 expression and upregulation of BAX expression levels. Our study suggests lobaplatin inhibits prostate cancer proliferation and migration through regulation of BCL2 and BAX expression.

scholarly journals miR-491 inhibits BGC-823 cell migration via targeting HMGA2

2019 ◽  
Vol 34 (4) ◽  
pp. 364-372 ◽  
Author(s):  
Zhigang Liu ◽  
Yun Lü ◽  
Qiuyu Jiang ◽  
Yang Yang ◽  
Chengxue Dang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Patients ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Cancer Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Gastric Cancer Patients ◽  
Proliferation And Migration

Purpose: miR-491 functions as a tumor suppressor in several types of cancer. However, its function and mechanism in gastric cancer proliferation and metastasis have not been well defined. The aim of this study was to explore the role and regulatory mechanism of miR-491 in cell proliferation and migration in gastric cancer. Methods: Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to detect the expression pattern of miR-491 in gastric cancer tissues. miR-491 overexpression vector, miR-491 inhibitor, and siHMGA2 were used; and MTT, wound healing, and transwell assays were employed to examine proliferation and migration for BGC-823 cells. A dual-luciferase reporter gene was used to measure the target relationship between miR-491 and HMGA2. Results: Most gastric cancer patients exhibit decreased miR-491 expression. miR-491 overexpression inhibited cell proliferation and migration, whereas miR-491 inhibitor treatment produced the opposite effect. Mechanistically, HMGA2 was identified as a direct target of miR-491. Moreover, HMGA2 knockdown inhibited cell proliferation and migration, which was similar to the effect of miR-491 overexpression. HMGA2 was decreased after transfection of the miR-491 vector and increased after transfection of the miR-491 inhibitor. Conclusion: Our results suggest that miR-491 suppressed cell proliferation and cell motility in gastric cancer by targeting HMGA2. Silencing HMGA2 produced a similar effect to miR-491 overexpression on cell proliferation and migration. miR-491/HMGA2 signaling may be a potential therapeutic target for gastric cancer patients with decreased miR-491 expression.

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