GINS2 was regulated by lncRNA XIST/miR-23a-3p to mediate proliferation and apoptosis in A375 cells

Hao, Yuqin; Liu, Kewei; Zhang, Xin; Kang, Shuxia; Zhang, Kun; Han, Wurihan; Li, Li; Li, Zhehai

doi:10.1007/s11010-020-04007-y

Cited by 11 publications

(6 citation statements)

References 36 publications

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“…Growing evidence has revealed that lncRNAs play crucial roles in the regulation of melanoma pathogenesis. To be specific, XIST, which is a lncRNA located on the X chromosome, is highly expressed and contributes to the progression of melanoma by sponging miRNA-23a-3p and indirectly targeting GINS2 ( 38 ). In addition, FUT8-AS1 functions as a tumor suppressor and inhibits proliferation, migration, and invasion of melanoma cells via binding to NF90, resulting in down-regulation of NRAS ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA CD27-AS1-208 Facilitates Melanoma Progression by Activating STAT3 Pathway

Shi

Guo

et al. 2022

Front. Oncol.

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Melanoma is the most lethal skin cancer that originates from epidermal melanocytes. Recently, long non-coding RNAs (lncRNAs) are emerging as critical regulators of cancer pathogenesis and potential therapeutic targets. However, the expression profile of lncRNAs and their role in melanoma progression have not been thoroughly investigated. Herein, we firstly obtained the expression profile of lncRNAs in primary melanomas using microarray analysis and unveiled the differentially-expressed lncRNAs compared with nevus. Subsequently, a series of bioinformatics analysis showed the great involvement of dysregulated lncRNAs in melanoma biology and immune response. Further, we identified lncRNA CD27-AS1-208 as a novel nuclear-localized factor with prominent facilitative role in melanoma cell proliferation, invasion and migration. Mechanistically, CD27-AS1-208 could directly interact with STAT3 and contribute to melanoma progression in a STAT3-dependent manner. Ultimately, the role of CD27-AS1-208 in melanoma progression in vivo was also investigated. Collectively, the present study offers us a new horizon to better understand the role of lncRNAs in melanoma pathogenesis and demonstrates that CD27-AS1-208 up-regulation contributes to melanoma progression by activating STAT3 pathway. Targeting CD27-AS1-208 in melanoma cells can be exploited as a potential therapeutic approach that needs forward validation in clinical trials in the future.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA CD27-AS1-208 Facilitates Melanoma Progression by Activating STAT3 Pathway

Shi

Guo

et al. 2022

Front. Oncol.

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“…Downregulation of GINS2 induces cell cycle arrest and apoptosis in lung cancer A549 cells ( 32 ). Silencing of GINS2, which is overexpressed in melanoma, inhibits cell proliferation and increases apoptosis in A375 cells ( 33 ). GINS2 interference induces cell cycle arrest and apoptosis of pancreatic cancer via the MAPK/ERK pathway ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

GINS2 regulates the proliferation and apoptosis of colon cancer cells through PTP4A1

Zhe

2022

Mol Med Rep

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colon cancer is associated with high death rates worldwide and poses a serious threat to public health. GinS complex subunit 2 (GinS2) serves a carcinogenic role in many cancers, including gastric adenocarcinoma, ovarian cancer and pancreatic cancer. However, the specific function of GINS2 in the development of colon cancer has not been described in detail. The present study aimed to clarify the role of GINS2 in colon cancer. a cell counting Kit-8 assay, edu staining, TUNEL and flow cytometry analyses were performed to determine the levels of cell viability, proliferation and apoptosis and to evaluate the cell cycle. Through the analysis of BioGrid, a Protein-Protein interaction database, it was hypothesized that protein tyrosine phosphatase 4a1 (PTP4a1) is a protein that might interact with GinS2, which was then validated using a co-immunoprecipitation assay. mrna and protein levels were measured using reverse transcription-quantitative Pcr and western blotting, respectively. The results of the present study demonstrated that GinS2 expression levels were increased in colon cancer cells. Furthermore, GinS2 knockdown inhibited the proliferation of colon cancer cells, while the levels of cell cycle arrest and apoptosis were increased. By interacting with PTP4A1, GINS2 promoted the expression of PTP4A1, a novel p53 target. GinS2 knockdown was increased, while PTP4a1 overexpression decreased the protein level of p53. Notably, PTP4A1 overexpression partly reversed the effects of GINS2 downregulation on colon cancer cells. Therefore, the present study demonstrated that GINS2 regulated the proliferation and apoptosis of colon cancer cells through PTP4A1/p53 pathway, highlighting that GinS2 may serve as a novel molecular marker for colon cancer prevention and therapy.

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“…Hao et al ( 2021 ) revealed that XIST facilitated oncogenic behavior of melanomas by sequestering miR-23a-3p and indirectly targeting its downstream gene, GINS2, thus providing a potential target (Fig. 4 U).…”

Section: Xist In Various Human Tumorsmentioning

confidence: 99%

“…XCI is an epigenetic silencing of a random X chromosome in female cells to balance the level of X gene expression between males and females (Lyon 1972 ; Loda and Heard 2019 ). More recently, abnormal overexpression of XIST was identified in a variety of human malignant tumors, such as esophageal cancer (EC) (Wu et al 2017a ), gastric cancer (GC) (Chen et al 2016 ), colorectal cancer (CRC) (Zhang et al 2019a ), pancreatic cancer (Sun et al 2018a ), hepatocellular carcinoma (HCC) (Liu and Xu 2019 ), laryngeal cancer (Xiao et al 2019 ), lung cancer (Tantai et al 2015 ), glioma (Yao et al 2015 ), neuroblastoma (NB) (Zhang et al 2019b ), osteosarcoma (OS) (Li et al 2017 ), bladder cancer (BC) (Xu et al 2018a ), retinoblastoma (RB) (Lyu et al 2019 ), cervical cancer (CC) (Zhu et al 2018a ), thyroid cancer (Xu et al 2018b ), nasopharyngeal carcinoma (NPC) (Song et al 2016 ), melanoma (Hao et al 2021 ), and leukemia (Wang et al 2020a ). In our review, we have summarized the mechanism underlying XIST, as well as the clinical significance of XIST, in the occurrence and progression of tumors.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA XIST: a novel oncogene in multiple cancers

Yang

Fei

et al. 2021

Mol Med

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Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is an important lncRNA derived from the XIST gene in mammals. XIST is abnormally expressed in numerous tumors, in most of which XIST functions as an oncogene. XIST is involved in multiple aspects of carcinogenesis, including tumor onset, progression, and prognosis. In our review, we collected and analyzed the recent studies on the impact of XIST in human tumor development. The multilevel molecular functions of XIST in human tumors are comprehensively reviewed to clarify the pathologic mechanisms and to offer a novel direction for further study.

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GINS2 was regulated by lncRNA XIST/miR-23a-3p to mediate proliferation and apoptosis in A375 cells

Cited by 11 publications

References 36 publications

Long Non-Coding RNA CD27-AS1-208 Facilitates Melanoma Progression by Activating STAT3 Pathway

Long Non-Coding RNA CD27-AS1-208 Facilitates Melanoma Progression by Activating STAT3 Pathway

GINS2 regulates the proliferation and apoptosis of colon cancer cells through PTP4A1

Long non-coding RNA XIST: a novel oncogene in multiple cancers

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