miR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer

Yan, Meina; Yang, Xinxin; Shen, Rong; Wu, Cuixia; Wang, Hui; Ye, Qing; Yang, Ping; Zhang, Lubin; Chen, Miao; Wan, Bing; Zhang, Qinqin; Sheng, Xia; Lü, Xiaodong; Shao, Gang; Zhou, Xiaoming; Yu, Jun; Shao, Qixiang

doi:10.1038/s41419-018-1093-9

Cited by 35 publications

(35 citation statements)

References 38 publications

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“…In advanced cancer stages (III/IV), the level of miR-146b-5p expression was lower compared to earlier stages (I/II) [56]. In the cell line study, overexpression of miR-146b-5p enhanced ovarian cancer cell sensitivity to PAC and CIS [56]. Thus, miR-146b-5p downregulation seems to play a role in the resistance of ovarian cancer to cytotoxic drugs, especially to PAC.…”

Section: Discussionmentioning

confidence: 82%

“…Further studies report that low level of miR-146b-5p expression correlates with ovarian cancer progression. In advanced cancer stages (III/IV), the level of miR-146b-5p expression was lower compared to earlier stages (I/II) [56]. In the cell line study, overexpression of miR-146b-5p enhanced ovarian cancer cell sensitivity to PAC and CIS [56].…”

Section: Discussionmentioning

confidence: 85%

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The Significance of MicroRNAs Expression in Regulation of Extracellular Matrix and Other Drug Resistant Genes in Drug Resistant Ovarian Cancer Cell Lines

Kaźmierczak

Jopek

Sterzyńska

et al. 2020

IJMS

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Ovarian cancer rates the highest mortality among all gynecological malignancies. The main reason for high mortality is the development of drug resistance. It can be related to increased expression of drug transporters and increased expression of extracellular matrix (ECM) proteins. Our foremost aim was to exhibit alterations in the miRNA expression levels in cisplatin (CIS), paclitaxel (PAC), doxorubicin (DOX), and topotecan (TOP)-resistant variants of the W1 sensitive ovarian cancer cell line-using miRNA microarray. The second goal was to identify miRNAs responsible for the regulation of drug-resistant genes. According to our observation, alterations in the expression of 40 miRNAs were present. We could observe that, in at least one drug-resistant cell line, the expression of 21 miRNAs was upregulated and that of 19 miRNAs was downregulated. We identified target genes for 22 miRNAs. Target analysis showed that miRNA regulates key genes responsible for drug resistance. Among others, we observed regulation of the ATP-binding cassette subfamily B member 1 gene (ABCB1) in the paclitaxel-resistant cell line by miR-363 and regulation of the collagen type III alpha 1 chain gene (COL3A1) in the topotekan-resistant cell line by miR-29a.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 85%

The Significance of MicroRNAs Expression in Regulation of Extracellular Matrix and Other Drug Resistant Genes in Drug Resistant Ovarian Cancer Cell Lines

Kaźmierczak

Jopek

Sterzyńska

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…In advanced cancer stage (III/IV) the level of miR-146b-5p expression was lower compared to earlier stage (I, II) [62]. In cell line study overexpression of miR-146b-5p enhanced ovarian cancer cell sensitivity to PAC and CIS [62]. Thus, miR-146b-5p downregulation seems to play a role in resistance of ovarian cancer to cytotoxic drugs, especially to PAC.…”

Section: Discussionmentioning

confidence: 86%

“…Further studies report that low level of miR-146b-5p expression correlates with ovarian cancer progression. In advanced cancer stage (III/IV) the level of miR-146b-5p expression was lower compared to earlier stage (I, II) [62]. In cell line study overexpression of miR-146b-5p enhanced ovarian cancer cell sensitivity to PAC and CIS [62].…”

Section: Discussionmentioning

confidence: 89%

The significance of microRNA genes expression in ovarian cancer cell lines resistant to cytotoxic drugs

Kaźmierczak¹,

Jopek²,

Sterzyńska³

et al. 2019

Preprint

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Ovarian cancer is the most fatal type of gynecological cancer. The main reason for high mortality is the development of drug resistance. It can be related to increased expression of drug transporters and increased expression of extracellular matrix (ECM) proteins. miRNA is a short noncoding RNA that regulates expression of about 60% of genes in the human genome and plays a crucial role in developing cancer, including resistance to chemotherapy.Our foremost aim was to exhibit alterations in the miRNA expression levels in the cisplatin (CIS), paclitaxel (PAC), doxorubicin (DOX), and topotecan (TOP) -resistant variants of W1 sensitive ovarian cancer cell line using miRNA microarray. The second goal was to identify miRNAs responsible for the regulation of drug-resistant genes.According to our observation, alterations in the expression of 40 miRNA genes. The level of expression of 21 genes was upregulated in at least one drug-resistant cell line. The expression of 19 genes was downregulated in at least one drug-resistant cell line. We identified target genes for 22 miRNAs. Target analysis showed that miRNA regulates key genes responsible for drug resistance. Among others, we observed regulation of the ABCB1 (MDR1) gene in the W1PR1 cell line by miR-363 and regulation of the COL3A1 gene in the W1TR cell line by miR-29a.Hence, on the basis of our findings, results indicate that genes responsible for drug resistance development in ovarian cancer can be regulated by miRNA.

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“…Also, FBXL10 was the direct target of miR-146b in regulating ovarian cancer cell proliferation, migration and invasion (12). Moreover, there were reports showed that miR-146b could regulate MyD88 expression in the proinflammatory response (13,14).…”

Section: Introductionmentioning

confidence: 99%

MiR-146b protects against pediatric pneumonia progression through MyD88/NF-κB signaling pathway

Zhang

Dong

Tang

et al. 2019

Preprint

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Background Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of children death. The present study was aimed to explore the role of miR-146b and its underlying mechanism in lipopolysaccharide (LPS)-induced inflammation injury in pediatric pneumonia. Methods Human fibroblasts WI-38 cells treated with LPS were subjected to construct cell model with inflammation injury. QRT-PCR or Western blot was applied to detect miR-146b and MyD88 expression. ELISA kit was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot. Results We displayed that miR-146b was downregulated, whereas MyD88 was upregulated in children with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumonia patients and WI-38 cells. Also, elevating miR-146b expression increased cell viability and reduced cell apoptosis. However, MyD88 overturned the protective effect of miR-146b on inflammation injury in pediatric pneumonia. Moreover, miR-146b overexpression inhibited the activation of NF-κB signaling pathway by suppressing MyD88. Conclusions These findings revealed that miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway.

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miR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer

Cited by 35 publications

References 38 publications

The Significance of MicroRNAs Expression in Regulation of Extracellular Matrix and Other Drug Resistant Genes in Drug Resistant Ovarian Cancer Cell Lines

The Significance of MicroRNAs Expression in Regulation of Extracellular Matrix and Other Drug Resistant Genes in Drug Resistant Ovarian Cancer Cell Lines

The significance of microRNA genes expression in ovarian cancer cell lines resistant to cytotoxic drugs

MiR-146b protects against pediatric pneumonia progression through MyD88/NF-κB signaling pathway

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