STAT1 mediated long non-coding RNA LINC00504 influences radio-sensitivity of breast cancer via binding to TAF15 and stabilizing CPEB2 expression

Feng, Jinchun; Li, Yan; Zhu, Ling; Zhao, Qian; Li, Dan; Li, Yuxiang; Wu, Tao

doi:10.1080/15384047.2021.1964320

Cited by 15 publications

(7 citation statements)

References 27 publications

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“…STAT1 has previously, mainly been studied in breast cancer (29). In breast cancer, STAT1 can be activated by numerous receptors, and it enhances the metastasis, invasion and proliferation of breast cancer cells (30). In the present study, STAT1 was highly expressed in OSCC and acted on the promoter region of BST2 to regulate BST2 expression.…”

Section: Discussionmentioning

confidence: 53%

BST2 regulated by the transcription factor STAT1 can promote metastasis, invasion and proliferation of oral squamous cell carcinoma via the AKT/ERK1/2 signaling pathway

Shan

Shen

Wang³

et al. 2023

Int J Oncol

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Oral squamous cell carcinoma (OSCC) is one of the main types of head and neck squamous cell carcinoma. Although progress has been made in treating OSCC, it remains a threat to human health, and novel therapeutic strategies are needed to extend the lifespan of patients with OSCC. The present study, evaluated whether bone marrow stromal antigen 2 (BST2) and STAT1 were potential therapeutic targets in OSCC. Small interfering RNA (siRNA) or overexpression plasmids were used to regulate BST2 or STAT1 expression. Western blotting and reverse transcription-quantitative PCR were performed to assess changes in the protein and mRNA expression levels of signaling pathway components. The effects of BST2 and STAT1 expression changes on the migration, invasion and proliferation of OSCC cells were assessed using the scratch test assay, Transwell assay and colony formation assay in vitro, respectively. Cell-derived xenograft models were used to evaluate the impact of BST2 and STAT1 on the occurrence and development of OSCC in vivo. Finally, it was demonstrated that BST2 expression was significantly upregulated in OSCC. Furthermore, it was demonstrated that high expression of BST2 in OSCC contributed to the metastasis, invasion and proliferation of OSCC cells. Moreover, it was demonstrated that the promoter region of BST2 was regulated by the transcription factor STAT1, and that the STAT1/BST2 axis could affect the behavior of OSCC via the AKT/ERK1/2 signaling pathway. In vivo studies also demonstrated that STAT1 downregulation inhibited OSCC growth by down-regulating BST2 expression via the AKT/ERK1/2 signaling pathway.

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Section: Discussionmentioning

confidence: 53%

BST2 regulated by the transcription factor STAT1 can promote metastasis, invasion and proliferation of oral squamous cell carcinoma via the AKT/ERK1/2 signaling pathway

Shan

Shen

Wang³

et al. 2023

Int J Oncol

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“…LINC00504-mediated TAF15 induced stability of CPEB2. Expression levels of CPEB2 mRNA were found to be reduced in LINC00504 knockdown or TAF15 depleted breast cancer cells treated with actinomycin D. Collectively, these findings indicated that stability of CPEB2 was evidently reduced upon the depletion of LINC00504 or TAF15 [ 18 ].…”

Section: Transcriptional Regulation Of Oncogenic Lncrnas By Stat1mentioning

confidence: 99%

Interplay between JAK/STAT pathway and non-coding RNAs in different cancers

Farooqi,

Shepetov,

Rakhmetova

et al. 2024

Non-coding RNA Research

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“…The examined lncRNA could affect DNA damage through its influence on ATM/ATR activation. LINC00504 depletion weakened the survival rate of BC cells, which was further enhanced by applied IR, suggesting its therapeutic potential [ 59 ]. Moreover, Wang et al discovered different lncRNA, whose downregulation could significantly improve BC patients’ response to radiotherapy.…”

Section: Involvement Of Lncrnas In Radiobiological Processesmentioning

confidence: 99%

Radio-lncRNAs: Biological Function and Potential Use as Biomarkers for Personalized Oncology

Kozłowska-Masłoń

Guglas

Paszkowska

et al. 2022

JPM

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Long non-coding RNAs (lncRNAs) consist of at least 200 nucleotides. Although these molecules do not code proteins, they carry many regulatory functions in normal cells, as well as in cancer cells. For instance, many of these molecules have been previously correlated with tumorigenesis of different cancers and their reaction to various stress factors, such as radiotherapy, chemotherapy, or reactive oxygen species (ROS). The lncRNAs are associated not only with dysregulation in cancers after applied treatment but also with beneficial effects that may be achieved by modulating their expression, often significantly enhancing the patients’ outcomes. A multitude of these molecules was previously considered as potential biomarkers of tumor development, progression, or cells’ response to radio- or chemotherapy. Irradiation, which is often used in treating numerous cancer types, is not always sufficient due to cells gaining resistance in multiple ways. In this review, studies considering lncRNAs and their reaction to radiotherapy were examined. These molecules were divided regarding their role in specific processes strictly related to irradiation, and their influence on this type of treatment was explained, showing how vast an impact they have on IR-supported combat with the disease. This review aims to shed some light on potential future lncRNA-based biomarkers and therapeutic targets.

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STAT1 mediated long non-coding RNA LINC00504 influences radio-sensitivity of breast cancer via binding to TAF15 and stabilizing CPEB2 expression

Cited by 15 publications

References 27 publications

BST2 regulated by the transcription factor STAT1 can promote metastasis, invasion and proliferation of oral squamous cell carcinoma via the AKT/ERK1/2 signaling pathway

BST2 regulated by the transcription factor STAT1 can promote metastasis, invasion and proliferation of oral squamous cell carcinoma via the AKT/ERK1/2 signaling pathway

Interplay between JAK/STAT pathway and non-coding RNAs in different cancers

Radio-lncRNAs: Biological Function and Potential Use as Biomarkers for Personalized Oncology

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