Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin

Xu, Xiaohui; Zhou, Xin; Chen, Zhenju; Gao, Chao; Zhao, Luo; Cui, Yuming

doi:10.18632/aging.102673

Cited by 55 publications

(51 citation statements)

References 53 publications

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“… 27 LncRNAs, HAS2-AS1 and XIST, accelerate resistance to chemotherapy in NSCLC. 28 , 29 In this study, we found that LINC01089 overexpression inhibited the proliferation, migration, and invasion of A549 and SK-MES-1, suggesting that LINC01089 acts as an anti-oncogene to inhibit tumorigenesis and metastasis in NSCLC. A previous study found that LINC01089 inhibits cell invasion in vitro and tumor metastasis in vivo and acts as a tumor suppressor gene and prognostic biomarker in breast cancer and ovarian cancer.…”

Section: Discussionmentioning

confidence: 61%

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

Zhang¹,

Cai²,

Cai³

et al. 2020

CMAR

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Background: Long non-coding RNAs (lncRNAs), a class of endogenous non-coding RNAs, play an important role in the development and metastasis of non-small cell lung cancer (NSCLC). However, the function and mechanism of action of long intergenic nonprotein coding RNA 1089 (LINC01089) in NSCLC remains unclear. This study aimed to identify the role of LINC01089 in cell proliferation, migration, and invasion of NSCLC. Methods: Expression of LINC01089 and the relationship between LINC01089 and overall survival (OS) in NSCLC were determined using GEPIA 2.0. Similarly, microRNAs (miRNAs) that showed increased expression in NSCLC and correlated with OS were identified using the online OncomiR cancer database. Target miRNAs of LINC01089 were predicted using starBase. Cell models of LINC01089 and miR-3187-3p overexpression were constructed using transfection. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to analyze the expression of LINC01089 and miR-3187-3p. MTS assay was used to assess cell proliferation. Transwell was used for migration and invasion assays. Results: LINC01089 expression was significantly reduced in NSCLC tissues and cells. Gain-of-function studies further demonstrated that LINC01089 overexpression inhibited proliferation, migration, and invasion of lung cancer cell lines, A549 and SK-MES-1. Based on starBase prediction and subsequent verification, we revealed that miR-3187-3p is a target miRNA of LINC01089. Additionally, miR-3187-3p expression was significantly increased in NSCLC tissues and cells. Overexpression of miR-3187-3p promoted proliferation, migration, and invasion of A549 and SK-MES-1 cells, thereby reversing the effect of LINC01089. Conclusion: LINC01089 attenuates tumor proliferation, migration, and invasion by sponging miR-3187-3p in NSCLC. LINC01089 acts as a tumor suppressor and represents a potential therapeutic target in NSCLC.

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Section: Discussionmentioning

confidence: 61%

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

Zhang¹,

Cai²,

Cai³

et al. 2020

CMAR

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“…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. Therefore, the relationship between XIST and pyroptosis was verified from multiple perspectives (61). In addition to NLRP3/caspase-1/ GSDMD pathway, the induction of GSDME cleavage in NSCLC causes pyroptosis and inhibits proliferation as well.…”

Section: Lung Cancermentioning

confidence: 96%

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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“…Emerging evidence has shown that DDP could induce pyroptotic cell death in various cells 9 , 29 . Enhancing the pyroptotic effect can increase the chemosensitivity to DDP in several cancer cells, including esophageal cancer cells 30 , oesophageal squamous cell carcinoma cells 31 , gastric cancer cells 29 , and non-small cell lung cancer cells 32 . Nevertheless, it is still unclear whether DDP induces TNBC cell pyroptosis.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin Induces Pyroptosis via Activation of MEG3/NLRP3/caspase-1/GSDMD Pathway in Triple-Negative Breast Cancer

Yan¹,

Luo²,

Wu³

et al. 2021

Int. J. Biol. Sci.

155

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Cisplatin (DDP) was reported to improve pathological complete response (pCR) rates in triple-negative breast cancer (TNBC) patients, however, the molecular mechanism still remains largely unknown. Emerging evidence suggested that some chemotherapeutic drugs played anti-tumor effects by inducing cell pyroptosis. Nevertheless, whether pyroptosis contributes to the DDP-induced anti-tumor effect in TNBC remains unexploited. In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo , providing evidence that DDP might induce pyroptosis in TNBC. Moreover, DDP activated NLRP3/caspase-1/GSDMD pyroptosis pathway by up-regulating the long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3). Furthermore, knockdown of MEG3 not only partly abolished the activation effect of DDP on NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis, but also reversed the suppression of DDP on tumor growth and metastasis ability in vitro and in vivo, further confirming that MEG3 may partially mediate the pyroptotic signaling upon DDP treatment. Thus, our data uncovered a novel mechanism that DDP induced pyroptosis via activation of MEG3/NLRP3/caspase-1/GSDMD pathway in TNBC to exert anti-tumor effects, which may help to develop new strategies for the therapeutic interventions in TNBC.

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Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin

Cited by 55 publications

References 53 publications

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

Cisplatin Induces Pyroptosis via Activation of MEG3/NLRP3/caspase-1/GSDMD Pathway in Triple-Negative Breast Cancer

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