scholarly journals Nomegestrol Acetate Suppresses Human Endometrial Cancer RL95-2 Cells Proliferation In Vitro and In Vivo Possibly Related to Upregulating Expression of SUFU and Wnt7a

2017 ◽  
Vol 18 (7) ◽  
pp. 1337 ◽  
Author(s):  
A-ying Ma ◽  
Shu-wu Xie ◽  
Jie-yun Zhou ◽  
Yan Zhu
Keyword(s):  
Endometrial Cancer ◽  
Nomegestrol Acetate ◽  
Proliferation In Vitro

miR-142 Suppresses Endometrial Cancer Proliferation In Vitro and In Vivo by Targeting Cyclin D1

2019 ◽  
Vol 38 (2) ◽  
pp. 144-150 ◽  
Author(s):  
Yi Su ◽  
Jing Wang ◽  
Zhao Ma ◽  
Wenjing Gong ◽  
Lianzhi Yu
Keyword(s):  
Endometrial Cancer ◽  
Cyclin D1 ◽  
Cancer Proliferation ◽  
Proliferation In Vitro

scholarly journals Metformin Enhances Nomegestrol Acetate Suppressing Growth of Endometrial Cancer Cells and May Correlate to Downregulating mTOR Activity In Vitro and In Vivo

2019 ◽  
Vol 20 (13) ◽  
pp. 3308 ◽  
Author(s):  
Can Cao ◽  
Jie-yun Zhou ◽  
Shu-wu Xie ◽  
Xiang-jie Guo ◽  
Guo-ting Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endometrial Cancer ◽  
Translation Initiation Factor ◽  
Cell Counting ◽  
Initiation Factor ◽  
Antitumor Effects ◽  
Nomegestrol Acetate ◽  
Ec Cells

This study investigated the effect of a novel progestin and its combination with metformin on the growth of endometrial cancer (EC) cells. Inhibitory effects of four progestins, including nomegestrol acetate (NOMAC), medroxyprogesterone acetate, levonorgestrel, and cyproterone acetate, were evaluated in RL95-2, HEC-1A, and KLE cells using cell counting kit-8 assay. Flow cytometry was performed to detect cell cycle and apoptosis. The activity of Akt (protein kinase B), mTOR (mammalian target of rapamycin) and its downstream substrates 4EBP1 (4E-binding protein 1) and eIF4G (Eukaryotic translation initiation factor 4G) were assayed by Western blotting. Nude mice were used to assess antitumor effects in vivo. NOMAC inhibited the growth of RL95-2 and HEC-1A cells, accompanied by arresting the cell cycle at G0/G1 phase, inducing apoptosis, and markedly down-regulating the level of phosphorylated mTOR/4EBP1/eIF4G in both cell lines (p < 0.05). Metformin significantly increased the inhibitory effect of and apoptosis induced by NOMAC and strengthened the depressive effect of NOMAC on activity of mTOR and its downstream substrates, compared to their treatment alone (p < 0.05). In xenograft tumor tissues, metformin (100 mg/kg) enhanced the suppressive effect of NOMAC (100 mg/kg) on mTOR signaling and increased the average concentration of NOMAC by nearly 1.6 times compared to NOMAC treatment alone. Taken together, NOMAC suppressing the growth of EC cells likely correlates to down-regulating the activity of the mTOR pathway and metformin could strengthen this effect. Our findings open a new window for the selection of progestins in hormone therapy of EC.

scholarly journals Locked nucleic acid-inhibitor of miR-205 decreases endometrial cancer cells proliferation in vitro and in vivo

Oncotarget ◽  
2016 ◽  
Vol 7 (45) ◽  
pp. 73651-73663 ◽  
Author(s):  
Anna Torres ◽  
Joanna Kozak ◽  
Agnieszka Korolczuk ◽  
Dominika Rycak ◽  
Paulina Wdowiak ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Nucleic Acid ◽  
Cancer Cells ◽  
Locked Nucleic Acid ◽  
Acid Inhibitor ◽  
Proliferation In Vitro

Ginkgolic acid induces apoptosis and autophagy of endometrial carcinoma cells via inhibiting PI3K/Akt/mTOR pathway in vivo and in vitro

2021 ◽  
pp. 096032712110237
Author(s):  
L Zhou ◽  
S Li ◽  
J Sun
Keyword(s):  
Endometrial Cancer ◽  
B Cells ◽  
Western Blot ◽  
Signal Pathway ◽  
Mtor Pathway ◽  
Related Protein ◽  
Western Blot Assay ◽  
Ginkgolic Acid

Endometrial cancer (EC) is the fourth most common malignancy in women in developed countries. The prognosis of EC is extremely poor, and it is an important factor that contributes to the death of patients. Therefore, studying EC pathogenesis and therapeutic targets, and exploring effective drugs are the primary tasks to improve the prognosis of EC. In the present study, we aimed to explore the function of ginkgolic acid (GA) in EC cell apoptosis and autophagy through PI3K/Akt/mTOR signal pathway in vitro and in vivo. Firstly, MTT assay and clone formation assay were employed to analyze the Ishikawa and HEC-1-B cell viabilities and proliferation after treatment with GA. The results showed that GA inhibited endometrial cancer cell survival. Flow cytometry assay and western blot assay were applied to examine the apoptosis and apoptosis related protein Bcl-2, Bax, Cleaved caspase-3 expression levels of Ishikawa and HEC-1-B cells after treatment with GA. Next, we applied western blot assay to analyze the autophagy associated proteins LC3I, LC3II, p62 and Beclin-1 in GA treated Ishikawa and HEC-1-B cells. We found that GA promoted apoptosis and induced autophagy of endometrial cancer cells. Meanwhile, western blot assay was also used to determine the expression levels of the PI3K/Akt/mTOR signal pathway related protein and the results revealed that GA inhibited the activity of PI3K/Akt/mTOR pathway. Finally, we found that GA inhibited tumor growth in vivo through immunohistochemistry assay. In conclusion, GA induces apoptosis and autophagy of EC cells via inhibiting PI3K/Akt/mTOR pathway in vivo and vitro.

scholarly journals Inactivating Mutations of the IK Gene Weaken Ku80/Ku70-Mediated DNA Repair and Sensitize Endometrial Cancer to Chemotherapy

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2487
Author(s):  
Chao Gao ◽  
Guangxu Jin ◽  
Elizabeth Forbes ◽  
Lingegowda S. Mangala ◽  
Yingmei Wang ◽  
...  
Keyword(s):  
Dna Repair ◽  
Endometrial Cancer ◽  
Protein Interactions ◽  
Somatic Mutations ◽  
The Cancer Genome Atlas ◽  
Response To Chemotherapy ◽  
Tcga Dataset ◽  
Inactivating Mutations

IK is a mitotic factor that promotes cell cycle progression. Our previous investigation of 271 endometrial cancer (EC) samples from the Cancer Genome Atlas (TCGA) dataset showed IK somatic mutations were enriched in a cluster of patients with high-grade and high-stage cancers, and this group had longer survival. This study provides insight into how IK somatic mutations contribute to EC pathophysiology. We analyzed the somatic mutational landscape of IK gene in 547 EC patients using expanded TCGA dataset. Co-immunoprecipitation and mass spectrometry were used to identify protein interactions. In vitro and in vivo experiments were used to evaluate IK’s role in EC. The patients with IK-inactivating mutations had longer survival during 10-year follow-up. Frameshift and stop-gain were common mutations and were associated with decreased IK expression. IK knockdown led to enrichment of G2/M phase cells, inactivation of DNA repair signaling mediated by heterodimerization of Ku80 and Ku70, and sensitization of EC cells to cisplatin treatment. IK/Ku80 mutations were accompanied by higher mutation rates and associated with significantly better overall survival. Inactivating mutations of IK gene and loss of IK protein expression were associated with weakened Ku80/Ku70-mediated DNA repair, increased mutation burden, and better response to chemotherapy in patients with EC.

scholarly journals Micro/nano-textured hierarchical titanium topography promotes exosome biogenesis and secretion to improve osseointegration

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhengchuan Zhang ◽  
Ruogu Xu ◽  
Yang Yang ◽  
Chaoan Liang ◽  
Xiaolin Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Titanium Surface ◽  
Titanium Implants ◽  
Extracellular Secretion ◽  
Exosome Biogenesis ◽  
Marrow Mesenchymal Stem Cells ◽  
Proliferation In Vitro ◽  
Extracellular Environment

Abstract Background Micro/nano-textured hierarchical titanium topography is more bioactive and biomimetic than smooth, micro-textured or nano-textured titanium topographies. Bone marrow mesenchymal stem cells (BMSCs) and exosomes derived from BMSCs play important roles in the osseointegration of titanium implants, but the effects and mechanisms of titanium topography on BMSCs-derived exosome secretion are still unclear. This study determined whether the secretion behavior of exosomes derived from BMSCs is differently affected by different titanium topographies both in vitro and in vivo. Results We found that both micro/nanonet-textured hierarchical titanium topography and micro/nanotube-textured hierarchical titanium topography showed favorable roughness and hydrophilicity. These two micro/nano-textured hierarchical titanium topographies enhanced the spreading areas of BMSCs on the titanium surface with stronger promotion of BMSCs proliferation in vitro. Compared to micro-textured titanium topography, micro/nano-textured hierarchical titanium topography significantly enhanced osseointegration in vivo and promoted BMSCs to synthesize and transport exosomes and then release these exosomes into the extracellular environment both in vitro and in vivo. Moreover, micro/nanonet-textured hierarchical titanium topography promoted exosome secretion by upregulating RAB27B and SMPD3 gene expression and micro/nanotube-textured hierarchical titanium topography promoted exosome secretion due to the strongest enhancement in cell proliferation. Conclusions These findings provide evidence that micro/nano-textured hierarchical titanium topography promotes exosome biogenesis and extracellular secretion for enhanced osseointegration. Our findings also highlight that the optimized titanium topography can increase exosome secretion from BMSCs, which may promote osseointegration of titanium implants.

Effects of retinoic acid steroidal analogs on human leukemic HL60 cell proliferation in vitro and on angiogenesis in vivo

2005 ◽  
Vol 16 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Evaggelia S. Arsenou ◽  
Evangelia P. Papadimitriou ◽  
Eleni Kliafa ◽  
Maria Hountala ◽  
Sotiris S. Nikolaropoulos
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Hl60 Cell ◽  
Proliferation In Vitro

scholarly journals Anti-angiogenic compound (TNP-470) inhibits mesangial cell proliferation in vitro and in vivo

1997 ◽  
Vol 51 (6) ◽  
pp. 1838-1846 ◽  
Author(s):  
Masashi Haraguchi ◽  
Mikio Okamura ◽  
Masayo Konishi ◽  
Yoshio Konishi ◽  
Nobuo Negoro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Proliferation In Vitro

Abstract 277: Microrna-33 Promotes Cardiac Fibrosis by Maintaining Cellular Lipid Homeostasis

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Masataka Nishiga ◽  
Takahiro Horie ◽  
Yasuhide Kuwabara ◽  
Osamu Baba ◽  
Tetsushi Nakao ◽  
...  
Keyword(s):  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Pressure Overload ◽  
Cholesterol Content ◽  
Atp Binding Cassette Transporter ◽  
Primary Fibroblasts ◽  
Proliferation In Vitro ◽  
Altered Lipid

Background: A highly conserved microRNA, miR-33 is considered as a potential therapeutic target for atherosclerosis, because recent reports, including ours, indicated miR-33 has atherogenic effects by reducing HDL-C. However, the functions of miR-33 in heart failure remain to be elucidated. Methods and results: To clarify the functions of miR-33 involved in cardiac hypertrophy and fibrosis in vivo, we investigated the responses to pressure overload by transverse aortic constriction (TAC) in miR-33 deficient (KO) mice. When subjected to TAC, miR-33 expression level was significantly up-regulated in wild-type (WT) left ventricles, whereas miR-33 KO hearts displayed no less hypertrophic responses than WT hearts. However, interestingly, histological and gene expression analyses showed ameliorated cardiac fibrosis in miR-33 KO hearts compared to WT hearts. Furthermore, we generated cardiac fibroblast specific miR-33 deficient mice, which also showed ameliorated cardiac fibrosis when they were subjected to TAC. We also found that cardiac fibroblasts were mainly responsible for miR-33 expression in the heart, because its expression was about 4-folds higher in isolated primary cardiac fibroblasts than cardiomyocytes. Deficiency of miR-33 impaired cell proliferation in primary fibroblasts, which was considered due to altered lipid raft cholesterol content by up-regulated ATP-binding cassette transporter A1/G1. Conclusion: Deficiency of miR-33 impaired fibroblast proliferation in vitro, and ameliorated cardiac fibrosis induced by pressure overload in vivo.

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