STAT1-Induced Upregulation lncRNA LINC00958 Accelerates the Epithelial Ovarian Cancer Tumorigenesis by Regulating Wnt/β-Catenin Signaling

Xie, Min; Fu, Qi; Wang, Pinpin; Cui, Yue

doi:10.1155/2021/1405045

Cited by 8 publications

(7 citation statements)

References 31 publications

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“…Yuan et al (61) demonstrated that STAT1 could be recruited into the promoter of β-catenin to activate its expression, and this effect was regulated by IFN-γ. In epithelial ovarian cancer, STAT1 could promote the upregulation of long non-coding RNA LINC00958, thus accelerating tumorigenesis by modulating Wnt/β-catenin signaling (62). A similar cross-link of STAT1 and Wnt/β-catenin signaling was also observed in the present study.…”

Section: Discussionsupporting

confidence: 87%

Exosomal STAT1 derived from high phosphorus‑stimulated vascular endothelial cells induces vascular smooth muscle cell calcification via the Wnt/β‑catenin signaling pathway

Zheng

et al. 2022

Int J Mol Med

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Vascular calcification is commonly observed in chronic kidney disease. The mechanism of how the calcification signal from endothelial cells is transmitted to vascular smooth muscle cells (VSMCs) remains unknown. The aim of the present study was to investigate whether exosomes from HUVECs (HUVEC-Exos) could regulate VSMC calcification and its potential signaling pathway. HUVEC-Exos were isolated from HUVECs under no phosphorus (NP) and high phosphorus (HP) conditions. Alizarin Red S staining and calcium (Ca) content analysis were carried out to detect calcification in VSMCs. Proteomics analysis was carried out to detect the differential expression of exosomal proteins. Protein and mRNA levels were measured by western blot analysis and reverse transcription-quantitative PCR (RT-qPCR). Exosomes derived from HP-HUVECs promoted the calcification of VSMCs, as assessed by Alizarin Red S staining, alkaline phosphatase activity assays, Ca content measurements and the increased expression of runt-related transcription factor 2 and osteopontin. Proteomic analysis detected the upregulation of STAT1 in HP-exosomes from HUVECs (HUVEC-Exos) compared with NP-HUVEC-Exos, which was also confirmed by western blot analysis and RT-qPCR. Inhibition of STAT1 expression in VSMCs using fludarabine or knockdown of STAT1 expression using small interfering RNA alleviated the calcification of VSMCs. Furthermore, lithium chloride (Wnt activator) reversed the protective effect of STAT1 inhibition on VSMC calcification, while Dickkopf-1 (Wnt inhibitor) exerted the opposite effect, suggesting that activation of the Wnt/β-catenin signaling pathway was involved in STAT1-mediated VSMC calcification. In conclusion, the present results indicated that exosomal STAT1 derived from HP-treated HUVECs could promote VSMC calcification, and activation of the Wnt/β-catenin pathway may be a potential mechanism of the VSMC calcification promoted by exosomes.

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Section: Discussionsupporting

confidence: 87%

Exosomal STAT1 derived from high phosphorus‑stimulated vascular endothelial cells induces vascular smooth muscle cell calcification via the Wnt/β‑catenin signaling pathway

Zheng

et al. 2022

Int J Mol Med

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“…1A ). Although carcinogenic functions have been previously identified in cervical cancer ( 38 ) and ovarian cancer ( 39 ), the role of BLACAT2 in UCEC remains unclear. BLACAT2 expression was therefore detected in clinical samples using RT-qPCR.…”

Section: Resultsmentioning

confidence: 99%

Long non‑coding RNA BLACAT2/miR‑378a‑3p/YY1 feedback loop promotes the proliferation, migration and invasion of uterine corpus endometrial carcinoma

Zhang

Wang

et al. 2023

Oncol Rep

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Uterine corpus endometrial carcinoma (UCEC) is a common gynecological malignancy with high rates of mortality and morbidity. The expression of long non-coding RNA bladder cancer-associated transcript 2 (BLACAT2) has been previously found to be aberrantly upregulated in UCEC. However, the regulatory consequences of this in UCEC progression remain poorly understood. In the present study, human UCEC cell lines AN3CA and HEC-1-A were infected with lentiviruses to overexpress BLACAT2 (Lv-BLACAT2) or knock down BLACAT2 using short hairpin RNA (Lv-shBLACAT2). BLACAT2 overexpression was found to promote the G 1 /S transition of cell cycle progression and UCEC cell proliferation. In addition, BLACAT2 overexpression was observed to facilitate UCEC cell migration and invasion. By contrast, BLACAT2 knockdown resulted in inhibitory effects in UCEC cell physiology. BLACAT2 overexpression also contributed to the activation of the MEK/ERK pathway. Subsequently, BLACAT2 was demonstrated to bind to microRNA (miR)-378a-3p according to dual-luciferase assays, where it appeared to function as a sponge of miR-378a-3p in 293T cells. miR-378a-3p overexpression was found to suppress UCEC cell proliferation, invasion, and ERK activation. Lentivirus-mediated knockdown of its target, the transcription factor Yin Yang-1 (YY1), was observed to reverse the oncogenic effects of BLACAT2 overexpression. Furthermore, YY1 was found to bind to the promoter of BLACAT2, suggesting that YY1 can regulate BLACAT2 expression. To conclude, results from the present study suggest that BLACAT2, miR-378a-3p and YY1 can form a feedback loop instead of an unidirectional axis, which can in turn regulate UCEC tumorigenesis through the MEK/ERK pathway. The present study furthered the understanding of UCEC tumorigenesis and may provide novel therapeutic targets for UCEC treatment.

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“…ISG20 promoted tumor progression in ccRCC and acted as a potential biomarker 16 . STAT1-induced upregulation lncRNA LINC00958 and promoted the tumorigenesis of OC via Wnt/β-Catenin signaling 17 . PSMA5 accelerated the tumorigenic process and involved in bortezomib resistance in prostate cancer 18 .…”

Section: Discussionmentioning

confidence: 99%

Machine learning developed a CD8+ exhausted T cells signature for predicting prognosis, immune infiltration and drug sensitivity in ovarian cancer

Chen,

Zheng,

Fei

et al. 2024

Sci Rep

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CD8+ exhausted T cells (CD8+ Tex) played a vital role in the progression and therapeutic response of cancer. However, few studies have fully clarified the characters of CD8+ Tex related genes in ovarian cancer (OC). The CD8+ Tex related prognostic signature (TRPS) was constructed with integrative machine learning procedure including 10 methods using TCGA, GSE14764, GSE26193, GSE26712, GSE63885 and GSE140082 dataset. Several immunotherapy benefits indicators, including Tumor Immune Dysfunction and Exclusion (TIDE) score, immunophenoscore (IPS), TMB score and tumor escape score, were used to explore performance of TRPS in predicting immunotherapy benefits of OC. The TRPS constructed by Enet (alpha = 0.3) method acted as an independent risk factor for OC and showed stable and powerful performance in predicting clinical outcome of patients. The C-index of the TRPS was higher than that of tumor grade, clinical stage, and many developed signatures. Low TRPS score indicated a higher level of CD8+ T cell, B cell, macrophage M1, and NK cells, representing a relative immunoactivated ecosystem in OC. OC patients with low risk score had a higher PD1&CTLA4 immunophenoscore, higher TMB score, lower TIDE score and lower tumor escape score, suggesting a better immunotherapy response. Moreover, higher TRPS score indicated a higher score of cancer-related hallmarks, including angiogenesis, EMT, hypoxia, glycolysis, and notch signaling. Vitro experiment showed that ARL6IP5 was downregulated in OC tissues and inhibited tumor cell proliferation. The current study constructed a novel TRPS for OC, which could serve as an indicator for predicting the prognosis, immune infiltration and immunotherapy benefits for OC patients.

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STAT1-Induced Upregulation lncRNA LINC00958 Accelerates the Epithelial Ovarian Cancer Tumorigenesis by Regulating Wnt/β-Catenin Signaling

Cited by 8 publications

References 31 publications

Exosomal STAT1 derived from high phosphorus‑stimulated vascular endothelial cells induces vascular smooth muscle cell calcification via the Wnt/β‑catenin signaling pathway

Exosomal STAT1 derived from high phosphorus‑stimulated vascular endothelial cells induces vascular smooth muscle cell calcification via the Wnt/β‑catenin signaling pathway

Long non‑coding RNA BLACAT2/miR‑378a‑3p/YY1 feedback loop promotes the proliferation, migration and invasion of uterine corpus endometrial carcinoma

Machine learning developed a CD8+ exhausted T cells signature for predicting prognosis, immune infiltration and drug sensitivity in ovarian cancer

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