Prostaglandin receptor EP3 regulates cell proliferation and migration with impact on survival of endometrial cancer patients

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.

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Should safety of the flu vaccine for cancer patients be reexamined?

F1000Research ◽

10.12688/f1000research.13428.1 ◽

2018 ◽

Vol 7 ◽

pp. 1 ◽

Cited By ~ 4

Author(s):

Slobodan Paessler ◽

Veljko Veljkovic

Keyword(s):

Experimental Data ◽

Cell Proliferation ◽

Influenza Vaccine ◽

Cancer Patients ◽

Influenza Infection ◽

Cell Proliferation And Migration ◽

Seasonal Flu ◽

Flu Vaccine ◽

And Migration ◽

Proliferation And Migration

Seasonal flu vaccine is recommended as the best protection for cancer patients against influenza infection. Recent in silico and experimental data suggest that antibodies elicited with influenza vaccine could activate bradykinin receptor B2-associated signaling pathway, which is also involved in cell proliferation and migration of tumor cells. These results point to an urgent need for the reexamination of safety of influenza vaccine(s) in cancer patients.

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

The International Journal of Biological Markers ◽

10.1177/1724600819874488 ◽

2019 ◽

Vol 34 (4) ◽

pp. 364-372 ◽

Cited By ~ 3

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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Ipatasertib, an oral AKT inhibitor, effectively inhibits cell proliferation and migration, and induces apoptosis in serous endometrial cancer cell lines in vitro: Endometrial Cancer Molecularly Targeted Therapy Consortium

Gynecologic Oncology ◽

10.1016/s0090-8258(21)01015-5 ◽

2021 ◽

Vol 162 ◽

pp. S192-S193

Author(s):

Lindsey Buckingham ◽

Jillian O'Donnell ◽

Tianran Hao ◽

Angeles Alvarez-Secord ◽

Chunxiao Zhou ◽

...

Keyword(s):

Cell Proliferation ◽

Endometrial Cancer ◽

Targeted Therapy ◽

Akt Inhibitor ◽

Endometrial Cancer Cell ◽

Molecularly Targeted Therapy ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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Forkhead box transcription factor, forkhead box A1, shows negative association with lymph node status in endometrial cancer, and represses cell proliferation and migration of endometrial cancer cells

Cancer Science ◽

10.1111/j.1349-7006.2012.02201.x ◽

2012 ◽

Vol 103 (4) ◽

pp. 806-812 ◽

Cited By ~ 21

Author(s):

Yayoi Abe ◽

Nobuhiro Ijichi ◽

Kazuhiro Ikeda ◽

Hidekazu Kayano ◽

Kuniko Horie-Inoue ◽

...

Keyword(s):

Cell Proliferation ◽

Transcription Factor ◽

Endometrial Cancer ◽

Lymph Node ◽

Negative Association ◽

Lymph Node Status ◽

Forkhead Box ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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ZIC2 upregulates lncRNA SNHG12 expression to promote endometrial cancer cell proliferation and migration by activating the Notch signaling pathway

Molecular Medicine Reports ◽

10.3892/mmr.2021.12271 ◽

2021 ◽

Vol 24 (3) ◽

Author(s):

Pengyu Cai ◽

Gaijuan Li ◽

Mingxiu Wu ◽

Bin Zhang ◽

Hong Bai

Keyword(s):

Cell Proliferation ◽

Endometrial Cancer ◽

Notch Signaling ◽

Cancer Cell ◽

Notch Signaling Pathway ◽

Cancer Cell Proliferation ◽

Endometrial Cancer Cell ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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Cholesterol as an Endogenous Ligand of ERRα Promotes ERRα-Mediated Cellular Proliferation and Metabolic Target Gene Expression in Breast Cancer Cells

Cells ◽

10.3390/cells9081765 ◽

2020 ◽

Vol 9 (8) ◽

pp. 1765

Author(s):

Faegheh Ghanbari ◽

Sylvie Mader ◽

Anie Philip

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Cell Proliferation ◽

Cancer Patients ◽

Dietary Cholesterol ◽

Breast Cancer Patients ◽

Endogenous Ligand ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

Breast cancer is the 2nd leading cause of cancer-related death among women. Increased risk of breast cancer has been associated with high dietary cholesterol intake. However, the underlying mechanisms are not known. The nuclear receptor, estrogen-related receptor alpha (ERRα), plays an important role in breast cancer cell metabolism, and its overexpression has been linked to poor survival. Here we identified cholesterol as an endogenous ligand of ERRα by purification from human pregnancy serum using a GST-ERRα affinity column and liquid chromatography-tandem mass spectrometry (LC-MS/MS). We show that cholesterol interacts with ERRα and induces its transcriptional activity in estrogen receptor positive (ER+) and triple negative breast cancer (TNBC) cells. In addition, we show that cholesterol enhances ERRα-PGC-1α interaction, induces ERRα expression itself, augments several metabolic target genes of ERRα, and increases cell proliferation and migration in both ER+ and TNBC cells. Furthermore, the stimulatory effect of cholesterol on metabolic gene expression, cell proliferation, and migration requires the ERRα pathway. These findings provide a mechanistic explanation for the increased breast cancer risk associated with high dietary cholesterol and possibly the pro-survival effect of statins in breast cancer patients, highlighting the clinical relevance of lowering cholesterol levels in breast cancer patients overexpressing ERRα.

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