Induction of apoptosis in ovarian cancer cells by miR-493-3p directly targeting AKT2, STK38L, HMGA2, ETS1 and E2F5

Kleemann, Michael; Schneider, Helga; Unger, Kristian; Bereuther, Jeremias; Fischer, Simon; Sander, Philip; Schneider, E. Marion; Fischer‐Posovszky, Pamela; Riedel, Christian U.; Handrick, René; Otte, Kerstin

doi:10.1007/s00018-018-2958-x

Cited by 29 publications

(34 citation statements)

References 68 publications

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“…8,20,27,28 Intriguingly, studies have noted that KDM3A could control the transcriptional activation of ETS1 in a similar manner. 9,29 ETS1 has been noted as an important oncogene and a treating target in multiple malignancies including breast cancer, 30,31 ovarian cancer, 32,33 and CC as well. 11,34 To validate this potential interaction between KDM3A and ETS1, we first identified nuclearlocalization of KDM3A and ETS1 in CC cells, and then a positive correlation between KDM3A and ETS1 was identified.…”

Section: Discussionmentioning

confidence: 99%

Histone Demethylase KDM3A Promotes Cervical Cancer Malignancy Through the ETS1/KIF14/Hedgehog Axis

Liu¹,

Li²,

Zhang

et al. 2020

OTT

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Section: Discussionmentioning

confidence: 99%

Histone Demethylase KDM3A Promotes Cervical Cancer Malignancy Through the ETS1/KIF14/Hedgehog Axis

Liu¹,

Li²,

Zhang

et al. 2020

OTT

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“…Previous evidence suggested that miR-493 inhibits the biological behavior of lung tumor [14]. Meanwhile, miR-493 also acts as a suppressor in various cancers including colon cancer, bladder cancer, and ovarian cancer via multiple intracellular signaling pathways [15][16][17].…”

Section: Discussionmentioning

confidence: 99%

FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

Jiang

Zhou

Gao

et al. 2020

Journal of Oncology

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Aberrant expression of FAM64A was correlated with cell proliferation in various cancer types. We examined the expression of FAM64A and the upstream gene miR-493 in OS. The functions of miR-493 were revealed through extensive experiments. We found an increase of FAM64A gene and protein in OS tissues. Overexpression of FAM64A resulted in promoting tumor proliferation, migration, and invasion. The miR-493 targeted and negatively regulated FAM64A. Our data showed that upregulation of FAM64A in OS correlated with poor prognosis.

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“…20 E2F5 was upregulated in OC, and E2F5 promoted cell proliferation, mobility, and induced apoptosis. [20][21][22] Moreover, the data showed that miR-1271-5p suppressed E2F5 to inhibit OC progression. 23 These data indicated that E2F5 was a positive regulator for the development of OC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis

Wang¹,

Han²,

Hu³

2020

CMAR

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Background: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) were reported to be related to the development of ovarian cancer (OC). In this study, the functional mechanisms of lncRNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) and microRNA-1271-5p (miR-1271-5p) were explored in OC. Methods: The level of MALAT1, miR-1271-5p, or E2F transcription factor 5 (E2F5) was detected by qRT-PCR. MTT assay, flow cytometry analysis and transwell migration and invasion assays were performed to determine cell proliferation, apoptosis, migration and invasion, respectively. E2F5 protein expression was detected by Western blot. The interaction between miR-1271-5p and MALAT1 or E2F transcription factor 5 (E2F5) was confirmed by the dual-luciferase reporter assay. Results: MALAT1 and E2F5 level were increased, while miR-1271-5p level was decreased in cisplatin (DDP)-resistant OC tissues and cells. MALAT1 knockdown or miR-1271-5p upregulation decreased IC 50 of cisplatin, and inhibited cell proliferation, migration, invasion, and facilitated cell apoptosis in DDP-resistant OC cells. Moreover, MALAT1 sponged miR-1271-5p to upregulate E2F5 expression. Besides, MALAT1 knockdown decreased DDP resistance, inhibited cell proliferation, migration, invasion, and promoted cell apoptosis by sponging miR-1271-5p to downregulate E2F5 expression in DDP-resistant OC cell. Conclusion: We demonstrated that MALAT1 mediated DDP-resistant OC development through miR-1271-5p/E2F5 axis, providing the theoretical basis for OC therapy.

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Induction of apoptosis in ovarian cancer cells by miR-493-3p directly targeting AKT2, STK38L, HMGA2, ETS1 and E2F5

Cited by 29 publications

References 68 publications

<p>Histone Demethylase <em>KDM3A</em> Promotes Cervical Cancer Malignancy Through the <em>ETS1</em>/KIF14/Hedgehog Axis</p>

<p>Histone Demethylase <em>KDM3A</em> Promotes Cervical Cancer Malignancy Through the <em>ETS1</em>/KIF14/Hedgehog Axis</p>

FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

<p>LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis</p>

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