Transcription Factor p53 Suppresses Tumor Growth by Prompting Pyroptosis in Non-Small-Cell Lung Cancer

Zhang, Tianze; Li, Yongchao; Zhu, Ruidong; Song, Peng; Wei, Youlei; Tian, Li; Xu, Guohai

doi:10.1155/2019/8746895

Cited by 76 publications

(69 citation statements)

References 32 publications

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“…Transcription factor p53 overexpression triggers pyroptosis to suppress tumor growth in A549 tumor-bearing mice. In clinical trials, p53 expression level is positively related to pyroptosis in tumor tissue of NSCLC patients, implicating the potentiality of p53 on antitumor via induction of pyroptosis [20]. The studies provide new ideas to support pyroptosis as a novel mechanism of molecular-targeted drugs to exterminate oncogene-addicted tumor cells.…”

Section: Non-chemotherapy Drug-induced Pyroptosis Exerts Anticancer Ementioning

confidence: 86%

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Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Zheng

2020

IJMS

146

111

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Programmed Cell Death (PCD) is considered to be a pathological form of cell death when mediated by an intracellular program and it balances cell death with survival of normal cells. Pyroptosis, a type of PCD, is induced by the inflammatory caspase cleavage of gasdermin D (GSDMD) and apoptotic caspase cleavage of gasdermin E (GSDME). This review aims to summarize the latest molecular mechanisms about pyroptosis mediated by pore-forming GSDMD and GSDME proteins that permeabilize plasma and mitochondrial membrane activating pyroptosis and apoptosis. We also discuss the potentiality of pyroptosis as a therapeutic target in human diseases. Blockade of pyroptosis by compounds can treat inflammatory disease and pyroptosis activation contributes to cancer therapy.

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Section: Non-chemotherapy Drug-induced Pyroptosis Exerts Anticancer Ementioning

confidence: 86%

“…On the other hand, resisting cell death is the important hallmark of cancers [19]. Induction of cancer cell pyroptosis by various stimulations can eliminate malignant cells [20][21][22][23][24]. Although pyroptotic death is often harmful to normal tissues, it can be beneficial to cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Zheng

2020

IJMS

146

111

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“…Furthermore, P53 was significantly upregulated in LPS-induced A549 pyroptosis. In conclusion, P53 might promote pyroptosis via binding and activating NLRP3 directly (59). Noncoding RNA also participates in the canonical pyroptosis of NSCLC.…”

Section: Lung Cancermentioning

confidence: 89%

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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“…TP53 is a well-known tumor suppressor that induces growth arrest or apoptosis and involved in cell cycle regulation. 28 TP53 is downregulated in many types of tumors including non-small cell lung cancer, colorectal cancer, cervical cancer and ovarian cancer, [29][30][31][32][33][34] which can lead to a poor survival rate. Our results showed that TP53 was downregulated in OC tissues, and could be decreased by miR-183-5p mimics and restored by overexpressed LEMD1-AS1, respectively.…”

Section: Discussionmentioning

confidence: 99%

<p>LEMD1-AS1 Suppresses Ovarian Cancer Progression Through Regulating miR-183-5p/TP53 Axis</p>

Guo¹,

Qin²

2020

OTT

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Background/Aims: Long noncoding RNAs (lncRNAs) play a critical role in tumorigenesis and progression of ovarian cancer (OC). This study focused on the function and potential mechanism toward LEMD1-AS1 (LEMD1 antisense RNA 1) in the progression of ovarian cancer. Materials and Methods: The expression of LEMD1-AS1 in OC tissues was evaluated in TCGA and Gene Expression Omnibus datasets (GSE119056) and confirmed in OC cell lines via qRT-PCR (quantitative real-time polymerase chain reaction). Then, the location of LEMD1-AS1 in the cytoplasmic and nuclear RNAs extracted from OV cells was detected by qRT-PCR. Cell Counting Kit-8 (CCK-8), colony formation, wound-healing and transwell assays were applied to examine cell viability, proliferation, migration and invasion, respectively. Further, the effect of LEMD1-AS1 on OC tumor growth was determined via subcutaneous xenotransplanted tumor model. The potential target for LEMD1-AS1 was validated via dual-luciferase activity assay, RNA pull-down and RNA immunoprecipitation. Results: The expression of LEMD1-AS1 was decreased in OC tissues and cell lines. Forced overexpression of LEMD1-AS1 inhibited the proliferation, migration and invasion of ovarian cancer cells and transplanted tumor growth in nude mice. We found that LEMD1-AS1 was mainly located in the cytoplasm of OC cells and contained complementary sites of miR-183-5p. Mechanistically, our results showed that LEMD1-AS1 could directly interact with miR-183-5p and tumor protein p53 (TP53). The anti-tumor role of LEMD1-AS1 on OC progression depended on miR-183-5p-mediated TP53 expression. Conclusion: LEMD1-AS1 suppresses OC progression through sponging miR-183-5p and regulation of TP53, suggesting a novel biomarker and target for OC.

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Transcription Factor p53 Suppresses Tumor Growth by Prompting Pyroptosis in Non-Small-Cell Lung Cancer

Cited by 76 publications

References 32 publications

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Induction of Pyroptosis: A Promising Strategy for Cancer Treatment

<p>LEMD1-AS1 Suppresses Ovarian Cancer Progression Through Regulating miR-183-5p/TP53 Axis</p>

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