Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer

Peng, Wan-Xin; Huang, Jianguo; Yang, Liu; Gong, Aihua; Mo, Yin‐Yuan

doi:10.1186/s12943-017-0727-3

Cited by 182 publications

(131 citation statements)

References 49 publications

Supporting

Mentioning

130

Contrasting

Order By: Relevance

“…In our study, we found that CoCl 2 inactivated ERK while activated MAPK pathways while ROR overexpression reversed this trend shown by activation of ERK and inactivation of MAPK. Our study was consistent with the previous study that lncRNA ROR activated ERK pathway through in breast cancer [33]. Our study went further and unveiled one possible underlying in which miR-145 was involved in.…”

Section: Discussionsupporting

confidence: 92%

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Ge¹,

Liu²,

Liu³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) is a condition causing apnea and hypopnea. LncRNA-ROR revealed properties in regulating hypoxia response. Our study explored the roles of ROR in CoCl 2-induced hypoxia injury in HK-2 cells. HK-2 cells were treated with CoCl 2 to induce hypoxia injury. Cell viability, cell apoptosis and apoptotic proteins were detected using CCK-8, flow cytometry and western blot, respectively. The alter expression of ROR and miR-145 was achieved through transfection. Moreover, the expressions of HIF-a and ERK and MAPK related factors were examined using western blot. We found that CoCl 2 decreased cell viability and increased apoptosis as well as increased the expression of ROR. ROR overexpression increased cell viability, decreased cell apoptosis. ROR overexpression upregulated anti-apoptotic proteins Bcl-2 and decreased p53, Bax and cleaved-Caspase-3. ROR overexpression also increased the expression of HIF-a. On the opposite, ROR silence led to the opposite results as relative to ROR overexpression. ROR overexpression decreased expression of miR-145. Co-transfection with ROR overexpression and miR-145 impaired the promoting effects of ROR in CoCl 2 treated cells. ROR increased phosphorylation of ERK while decreased phosphorylation of MAPK. In conclusion, lncRNA ROR alleviated CoCl 2-induced hypoxia injury through regulation of miR-145 as well as modulating ERK and MAPK signalling. HIGHLIGHTS 1. CoCl 2 induces ROR upregulation; 2. Overexpression of ROR reduces CoCl 2-induced HK-2 cell injury; 3. Silence of ROR promotes CoCl 2-induced HK-2 cell injury; 4. Overexpression of ROR decreases miR-145 expression; 5. ROR overexpression modulates ERK and MAPK signalling pathways through regulation of miR-145.

show abstract

Section: Discussionsupporting

confidence: 92%

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Ge¹,

Liu²,

Liu³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

show abstract

“…Besides, it both inhibits p53 translation [42] and enhances c-Myc expression through interaction with heterogeneous nuclear ribonucleoprotein I (hnRNP I) [43]. While in triple negative breast cancer, linc-RoR increases cell invasion via miR-145/ ARF6 pathway [44], in estrogen receptor positive breast tumors it activates MAPK/ ERK pathway through diminish ing the stability of dual specificity phosphatase 7 (DUSP7) which down-regulates ERK [45].…”

Section: Lincrna Regulator Of Reprogramm Ing (Linc-ror)mentioning

confidence: 99%

Long Non-coding RNAs as Regulators of the Mitogen-activated Protein Kinase (MAPK) Pathway in Cancer

Tasharrofi¹,

Ghafouri‐Fard²

2018

Klin Onkol

View full text Add to dashboard Cite

Considering the role of this pathway in the pathogenesis of several cancers, alterations in lncRNA expression lead to changes in MAPK pathway resulting in inhibition of apoptosis and induction of cell proliferation and migration. Moreover, some lncRNAs participate in cross-talk between MAPK and other cancer-related pathways, such as PI3K/Akt pathway through regulation of certain shared proteins between these pathways. Based on the availability of certain anticancer drugs that modulate this pathway, identification of lncRNAs that affect this pathway would help in establishment of effective therapies.Key words: RNA - long noncoding - mitogen-activated protein kinases - signal transduction.

show abstract

“…linc-ROR is important in regulating epithelial-to-mesenchymal transition (EMT) and can promote breast cancer progression and metastasis through the regulation of miR-NAs (Hou et al, 2014). linc-ROR also functions as an onco-lncRNA to promote the estrogen-independent growth of ER-positive breast cancer and to contribute to tamoxifen resistance (Peng et al, 2017). linc-ROR is an important marker for multidrug resistance in breast cancer, and its upregulation is important for chemotherapy tolerance (Chen et al, 2016a), and it confers the resistance of breast cancer cells to gemcitabine by silencing miR-34a expression (Chen et al, 2016b).…”

Section: Introductionmentioning

confidence: 99%

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

et al. 2020

View full text Add to dashboard Cite

linc‐ROR is reported to be a potential biomarker of breast cancer, but the detailed mechanism of linc‐ROR‐mediated breast cancer regulation has not been fully studied. We aimed to explore how linc‐ROR affects proliferation, metastasis, and drug sensitivity in breast cancer. Cell lines in which linc‐ROR was overexpressed or knocked down were constructed, and the cell proliferation, colony formation, cell migration, and invasion abilities of these lines were explored. A CCK‐8 assay was performed to determine the sensitivity of the breast cancer cells to rapamycin. Next‐generation sequencing was conducted to explore the detailed regulatory mechanism of linc‐ROR; differentially expressed RNAs in the linc‐ROR‐overexpressing cell line compared with the negative control were screened out, and their target genes were chosen to perform Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis, protein–protein interaction network analysis, and competing endogenous RNA (ceRNA) network analysis. The ceRNA mechanism of linc‐ROR for miR‐194‐3p, which targets MECP2, was determined through dual‐luciferase reporter assay, RT–qPCR, western blot, and rescue experiments. Finally, we found that linc‐ROR was upregulated in breast tumor tissues. linc‐ROR promoted the cell proliferation, colony formation, cell migration, and invasion of breast cancer and decreased the sensitivity of breast cancer cells to rapamycin. The overexpression of linc‐ROR triggered changes in the whole transcriptome of breast cancer cells, and a total of 85 lncRNAs, 414 microRNAs, 490 mRNAs, and 92 circRNAs were differentially expressed in the linc‐ROR‐overexpressing cell line compared with the negative control. Through a series of bioinformatic analyses, the ‘linc‐ROR/miR‐194‐3p/MECP2’ ceRNA regulatory axis was confirmed to be involved in the linc‐ROR‐mediated progression and drug sensitivity of breast cancer. In conclusion, linc‐ROR serves as an onco‐lncRNA in breast cancer and promotes the survival of breast cancer cells during rapamycin treatment by functioning as a ceRNA sponge for miR‐194‐3p, which targets MECP2.

show abstract

Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer

Cited by 182 publications

References 49 publications

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Long Non-coding RNAs as Regulators of the Mitogen-activated Protein Kinase (MAPK) Pathway in Cancer

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

Contact Info

Product

Resources

About