Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Liu, Jinglei; Yao, Lei; Zhang, Mingyan; Ji, Jiang; Mi, Yang; Wang, Yue

doi:10.18632/aging.102291

Cited by 165 publications

(140 citation statements)

References 32 publications

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“…Thus, inhibiting LncRNA-XIST may contribute to the treatment of NSCLC patients. Subsequent experiments found that knocking down LncRNA-XIST led to pyroptosis by activating the miR-335/SOD2/ROS/ NLRP3 signal pathway (60). In another research, downregulation of LncRNA-XIST was demonstrated to relieve its suppression of Smad2 nuclear translocation, subsequently triggering transcriptional activation of P53 and NLRP3.…”

Section: Lung Cancermentioning

confidence: 97%

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

et al. 2021

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Pyroptosis, a lytic pro-inflammatory type of programmed cell death, has been widely studied in diverse inflammatory disease models. Membrane perforation and cell swelling induced by cleaved gasdermin family members is the main characteristic of pyroptosis. Emerging evidence has revealed a complicated relationship between pyroptosis and cancer. On the one hand, as inflammatory cell death, pyroptosis provides a comfortable environment for tumor proliferation. On the other hand, excessive activation of pyroptosis can inhibit the development of tumor cells. In this review, we first summarized the latest progress about the molecular mechanism of pyroptosis. Then, members from gasdermin family, the central molecules of pyroptosis which formed pores on the cell membrane, were highlighted. In the second part of this review, we summarized drugs that induced pyroptosis in different tumors and their concrete mechanisms based on recent literature reports. In the final section, we discussed several hotspots in pyroptosis and cancer therapy, which will point out the direction of sequent research. In brief, inducing pyroptosis in cancer cells is a promising strategy for cancer therapy.

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Section: Lung Cancermentioning

confidence: 97%

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

et al. 2021

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“…For instance, lncRNA XIST has been reported to regulate cell proliferation in non-small cell lung cancer by modulating miR-186-5p and miR-335/SOD2/ROS signaling pathways. 8,9 Moreover, lncRNA XIST has been shown to target miR-194-5p and miR-139-5p to regulate growth of hepatocellular carcinoma cells. 12,34 Further, lncRNA XIST has been demonstrated to promote proliferation of pancreatic cancer cells by acting as a sponge for miR-429 and miR-133a.…”

Section: Discussionmentioning

confidence: 99%

“…To normalize the values, each firefly luciferase value was divided by the value for renilla luciferase in the same well. 9,29 Tumor Xenograft Model…”

Section: Luciferase Activity Assaymentioning

confidence: 99%

“…7 Recently, lncRNA XIST has been shown to contribute to the development of various cancers, including non-small cell lung cancer, hepatocellular carcinoma, and pancreatic cancer. [8][9][10][11][12] Interestingly, the mechanism through which lncRNA XIST functions in these different types of cancers appear to involve similar regulation, in which lncRNA XIST acts as a sponge that can sequester miRNA and indirectly upregulate oncogene expression in these cancers. [8][9][10][11][12] The miRNAs involved are specific and dependent on the cancer type.…”

Section: Introductionmentioning

confidence: 99%

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<p>LncRNA XIST Promotes Growth of Human Chordoma Cells by Regulating miR-124-3p/iASPP Pathway</p>

Bai¹,

Pan²,

Du³

et al. 2020

OTT

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Introduction: Chordoma is a malignant primary bone tumor that is found in the spine and skull. X-inactive specific transcript (XIST) is a long non-coding RNA (lncRNA) is known to be involved in the development of various cancers, but its precise function and mechanism in human chordoma have not been elucidated. Here, we investigated the role of lncRNA XIST in chordoma progression. Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was performed to determine lncRNA XIST expression in human chordoma tissues and matched-noncancerous tissues. Western blot was used to determine protein expression. Silencing and overexpression of lncRNA XIST were carried out by RNA interference (RNAi) and lentiviral transduction, respectively. Cell Counting Kit-8 (CCK-8) assay and flow cytometry were employed to examine the effects of lncRNA XIST on growth of human chordoma cells. Lastly, the role of lncRNA XIST in vivo was explored using a xenograft model. Results: We found that lncRNA XIST expression was upregulated in chordoma and strongly correlated with poor patient prognosis. Moreover, lncRNA XIST promoted proliferation and inhibited apoptosis of chordoma cells. Mechanistically, upregulation of lncRNA XIST led to a decrease in miR-124-3p expression, thereby promoting the expression of the miR-124-3p target gene, inhibitor of apoptosis-stimulating protein of p53 (iASPP). Addition of miR-124-3p inhibitor or mimic reversed the effects induced by lncRNA XIST silencing or overexpression on chordoma cell proliferation. Lastly, using a xenograft mouse model, we found that silencing of lncRNA XIST decreased tumorigenicity in vivo, as shown by increased tumor cell apoptosis. Conclusion: Our findings demonstrate a key role for lncRNA XIST in chordoma progression by regulating miR124-3p/iAPSS pathway.

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“…However, the increasing evidence has revealed the multiple functions of lncRNAs on cell fate regulation, especially on tumorigenesis [11]. For example, lncRNA-MALAT1 [12,13] and lncRNA-XIST [14,15] have been elucidated to regulate the proliferation, invasion, and migration of NSCLC. Still, there have been a large amount of lncRNAs whose effects on NSCLC tumorigenesis have not been clearly identified.…”

Section: Introductionmentioning

confidence: 99%

LINC00476 suppresses the progression of non-small cell lung cancer via inducing the ubiquitination of SETDB1

Wang

Chen

et al. 2020

Preprint

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Background: Long non-coding RNAs are involved in the tumorigenesis of non-small cell lung cancer (NSCLC). This study aims to investigate whether LINC00476 affects the proliferation, invasion, and migration of NSCLC cells via SETDB1-activated Wnt/β-catenin pathway. Method: The expression of LINC00476, SETDB1, Wnt1, and β-catenin were determined in NSCLC tumor tissues and the paired adjacent tissues, as well as in NSCLC cell lines and bronchial epithelioid cell lines. Cell proliferation, invasion, and migration were determined using cell counting kit-8 assay and Transwell assay. The relationship between LINC00476 and SETDB1 was elucidated using RNA pull-down, RNA immunoprecipitation, and ubiquitination assays. Result: LINC00476 was significantly downregulated, while SETDB1, Wnt1, and β-catenin were upregulated in NSCLC tumor tissues and cell lines compared to the normal ones. Overexpression of LINC00476 promoted the proliferation, invasion, and migration of NSCLC cells, as well as suppressed tumor growth in the mouse xenograft. Meanwhile, overexpression of LINC00476 induced the degradation of SETDB1 via promoting its ubiquitination. The simultaneous overexpression of LINC00476 and SETDB1 negated the inhibition of LINC00476 overexpression on the proliferation, invasion, and migration of NSCLC cells. Conclusion: LINC00476 acts as a tumor suppressor in NSCLC via downregulating SETDB1, which provides a novel target in treating NSCLC.

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Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Cited by 165 publications

References 32 publications

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

<p>LncRNA XIST Promotes Growth of Human Chordoma Cells by Regulating miR-124-3p/iASPP Pathway</p>

LINC00476 suppresses the progression of non-small cell lung cancer via inducing the ubiquitination of SETDB1

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