The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

Lu, Dianxiang; Di, Shihao; Zhuo, Shuaishuai; Zhou, Lei; Bai, Rumeng; Zou, Zigui; Chen, Chunni; Sun, Menghong; Tang, Jinhai

doi:10.1038/s41420-021-00419-x

Cited by 19 publications

(11 citation statements)

References 32 publications

(54 reference statements)

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“…Previous studies have shown that high mRNA expression of OASL and OAS3 was associated with poor prognosis in all breast cancer patients [ 20 ]. Other studies have revealed that OASL was regulated by upstream long noncoding RNA TINCR to promote the metastasis of breast cancer [ 21 ]. Combined with these studies, it is suggested that ADAR may be involved in the OASL-related regulatory pathway.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of ADAR Promotes Breast Cancer Progression and Serves as a Potential Therapeutic Target

Sun

et al. 2021

Journal of Oncology

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Background. Breast cancer (BC) is the most common cause of cancer death worldwide, and its incidence is increasing every year. This study aims to investigate the expression characteristics of ADAR gene in breast cancer and to explore its role in the occurrence and development of BC and its possible mechanism. Methods. TCGA portal was used to detect the expression of ADAR in cancer including BC, and its correlation with clinicopathological data as well as other genes was analyzed via UALCAN database. The TISCH database evaluated the expression of ADAR in different types of cell populations in BC at the single-cell level. The Kaplan–Meier plotter database was used to predict the correlation between ADAR expression and BC patient prognosis. The Human Protein Atlas was used to detect the expression of ADAR in tissues and location of ADAR mRNA in cells. Moreover, the relationships between immune response and ADAR expression in BC were assessed with the use of the TISIDB. Metascape and STRING were applied to predict ADAR with other protein interactions. Finally, the effect generated by ADAR expression on cell proliferating, invading, and migrating processes was assessed in vitro with knockdown and overexpression strategies. Results. ADAR was significantly upregulated in BC tissues compared to paracancerous tissues. Single-cell RNA analysis showed that ADAR was specifically upregulated in cancer cell clusters and was also expressed in stromal and immune cell clusters. The upregulation of ADAR was positively correlated with clinicopathological stage and negatively correlated with BC prognosis. Experimental processes in vitro revealed ADAR knockdown hindered, proliferated, invaded, and migrated levels of BC cells, whereas over expression of ADAR played the opposite effect. ADAR protein, which may interact with OASL, STAT2, and IFIT3, was mainly located in the nucleoli in cells and primarily involved DNA modification and apoptotic signaling pathway. Immune factors may interact with ADAR in BC, and ADAR was found noticeably linked with immunosuppressor such as IL10, CD274, and IDO1. Conclusion. ADAR is significantly upregulated in breast cancer tissues, which may promote the progression of BC through the interaction of cancer cells, stromal cells, and immune cells. Targeting ADAR may offer new hope in treating breast cancer.

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Section: Discussionmentioning

confidence: 99%

Upregulation of ADAR Promotes Breast Cancer Progression and Serves as a Potential Therapeutic Target

Sun

et al. 2021

Journal of Oncology

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“…Based on these, we predicted that the interaction of lncRNA SNHG7 and EIF4G2 could affect the degradation of EIF4G2 to affect PTX-sensitivity of SKOV3-PTX or heyA8-PTX and some malignant behavior of these cells. It was reported that protein interacting with LncRNA could play a vital role in stabilizing LncRNA [ 29 , 30 ]. Maybe this interaction could affect the stability of lncRNA SNHG7, which required further investigated.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA (LncRNA) SNHG7/ Eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) involves in the malignant events of ovarian cancer cells with paclitaxel resistant

Zhang

2021

Bioengineered

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LncRNA SNHG7 shows a strong relationship with malignant behavior of cancer cells and poor clinical outcome in cancer. The resistance of ovarian cancer for Paclitaxel seriously limits the clinical efficacy in chemotherapy for ovarian cancer patients. In this study, we investigated whether lncRNA SNHG7 was involved in Paclitaxel sensitivity of ovarian cancer as well as the underlying mechanism regulating the behavior of ovarian cancer cells with Paclitaxel resistance. The experiment results of wound healing and transwell showed that in paclitaxel-resistant ovarian cancer cells, transfection with siRNA-SNHG7 in ovarian cancer cells reduced cell migration and invasion. And cell cycle was observed by means of Flow cytometry. RNA immunoprecipitation assay was performed to analyze the interaction of lncRNA SNHG7 and EIF4G2. Overexpression of EIF4G2 by transfection with Ov- EIF4G2 plasmids efficiently blocked the changes of migration and invasion, as well as G0/1 arrest caused by lncRNA SNHG7 silencing. Taken together, these results demonstrated that lncRNA SNHG7 could affect the degradation of EIF4G2 to regulate the sensitivity of ovarian cancer to Paclitaxel, inhibit cell viability, migration, and invasion. The interaction of lncRNA SNHG7 and EIF4G2 plays an important role in the migrative and invasive activity and Paclitaxel resistance of ovarian cancer cells.

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“…For example, PAST homolog 1 contributes to cell proliferation and cell cycle progression ( 32 , 33 ). Reduced expression of 2-5A synthase 1 by a non-coding RNA named TINCR facilitates proliferation in breast cancer cells ( 34 ). MARS has an important role in initiating translation and protection against cellular damage ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Role of AUF1 in modulating the proliferation, migration and senescence of skin cells

Wang

et al. 2021

Exp Ther Med

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AU-rich element RNA-binding factor 1 (AUF1) is a classical RNA-binding protein. AUF1 influences the process of development, apoptosis and tumorigenesis by interacting with adenylate-uridylate rich element-bearing mRNAs. Human skin is the largest organ of the body and acts as a protective barrier against pathogens and injuries. The aim of the present study was to explore the function and potential molecular pathways of AUF1 in human skin cells. AUF1 was overexpressed in human keratinocyte HaCaT cells and human skin fibroblast WS1 cells using adenoviruses and silenced using lentiviruses. AUF1 overexpression facilitated cell proliferation, whereas AUF1 knockdown induced the opposite effect. AUF1 reduced apoptosis but did not affect cell cycle progression. Forced AUF1 expression promoted the migration of human skin cells, as demonstrated by a scratch wound healing assay. Cell senescence was alleviated in AUF1-overexpressing skin cells, while AUF1 knockdown increased cell senescence. WS1 cells with AUF1 overexpression and silencing were used for RNA-sequencing and Kyoto Encyclopedia of Genes and Genomes-based pathway analysis to identify AUF1-affected mRNAs. A total of 18 mRNAs (eight mRNAs with positive associations and 10 mRNAs with negative associations) revealed consistent associations with both AUF1 overexpression and silencing. Enriched pathways associated with AUF1 expression included ‘MAPK’, ‘cell adhesion molecules’, ‘proteasome’, ‘cellular senescence’ and ‘TGF-β signaling’, indicating a complex regulatory network. Overall, the results of the present study revealed that AUF1 is involved in the proliferation, migration and senescence of skin cells in vitro and may be a potential target for cosmetic and disease treatment of skin.

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The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

Cited by 19 publications

References 32 publications

Upregulation of ADAR Promotes Breast Cancer Progression and Serves as a Potential Therapeutic Target

Upregulation of ADAR Promotes Breast Cancer Progression and Serves as a Potential Therapeutic Target

Long non-coding RNA (LncRNA) SNHG7/ Eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) involves in the malignant events of ovarian cancer cells with paclitaxel resistant

Role of AUF1 in modulating the proliferation, migration and senescence of skin cells

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