Biological functions and clinical significance of the newly identified long non‑coding RNA RP1‑85F18.6 in colorectal cancer

Ma, Yeshuo; Chen, Yifei; Lin, Changwei; Hu, Guoqing

doi:10.3892/or.2018.6694

Cited by 53 publications

(59 citation statements)

References 38 publications

(44 reference statements)

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“…In addition, compared to wild-type (WT) littermates, Casp11 −/− mice are highly vulnerable to the AOM/DSS model of CAC 70 . GSDMA was not expressed in normal colorectal epithelial cells but was gradually overexpressed in carcinoma cells, while GSDMD exhibited the opposite trend 71,72 . Gsdmc is not detected in normal colorectal tissues but is present in CRC tissues.…”

Section: Role Of Pyroptosis In Tumorigenesis and Metastasismentioning

confidence: 90%

The role of pyroptosis in cancer: pro-cancer or pro-“host”?

et al. 2019

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Programmed cell death (PCD) refers to the way in which cells die depending on specific genes encoding signals or activities. Apoptosis, autophagy, and pyroptosis are all mechanisms of PCD. Among these mechanisms, pyroptosis is mediated by the gasdermin family, accompanied by inflammatory and immune responses. The relationship between pyroptosis and cancer is complex, and the effects of pyroptosis on cancer vary in different tissues and genetic backgrounds. On one hand, pyroptosis can inhibit the occurrence and development of tumors; on the other hand, as a type of proinflammatory death, pyroptosis can form a suitable microenvironment for tumor cell growth and thus promote tumor growth. In addition, the induction of tumor pyroptosis is also considered a potential cancer treatment strategy. Studies have shown that DFNA5 (nonsyndromic hearing impairment protein 5)/GSDME (Gasdermin-E) mRNA methylation results in lower expression levels of DFNA5/GSDME in most tumor cells than in normal cells, making it difficult to activate the pyroptosis in most tumor cells. During the treatment of malignant tumors, appropriate chemotherapeutic drugs can be selected according to the expression levels of DFNA5/GSDME, which can be upregulated in tumor cells, thereby increasing the sensitivity to chemotherapeutic drugs and reducing drug resistance. Therefore, induced pyroptosis may play a predominant role in the treatment of cancer. Here, we review the latest research on the anti-and protumor effects of pyroptosis and its potential applications in cancer treatment. Facts Open questions 1. Does pyroptosis play differential roles in normal and tumor tissues? 2. What are the key signals that initiate pyroptosis? 3. What are the key signaling pathways impacted by pyroptosis in tumors? 4. How can pyroptosis be manipulated to drive tumor fate?

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Section: Role Of Pyroptosis In Tumorigenesis and Metastasismentioning

confidence: 90%

The role of pyroptosis in cancer: pro-cancer or pro-“host”?

et al. 2019

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“…The subsequent study showed that the effect of the pathway on the cell cycle was mediated by cyclin proteins. As cyclin A regulates the S phase [ 41 ] and cyclin B regulates the G2 phase[ 42 ], emodin decreased cyclin A and B which results in the decrease in cells at the S/G2 phase. Cyclin C was proved to suppressed cancer [ 43 ], it is also a downstream target of emodin found by this study.…”

Section: Discussionmentioning

confidence: 99%

Emodin regulates cell cycle of non-small lung cancer (NSCLC) cells through hyaluronan synthase 2 (HA2)-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway

Jin

Cao

et al. 2021

Cancer Cell Int

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Background Non-small cell lung cancers (NSCLC) account for most cases of lung cancer. More effort is needed to research new drug and combination therapies for this disease. An anthraquinone derivative, emodin shows anticancer potency. We hypothesis that emodin suppresses lung cancer cells through hyaluronan (HA) synthase 2-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway mediated cell cycle regulation. Methods We tested the effect of emodin on viability, apoptosis, and HA secretion of 5 NSCLC cell lines. We used NSCLC cells A549 for two rounds of knockdown study: (1) knocking down either the synthases (HAS2 and HAS3) or the receptors (CD44 and RHAMM); (2) knocking down either HAS2 or HAS3. Then determined the effect of emodin on viability, HA secretion, cell cycle, and expression of cyclin proteins. Results Emodin suppressed viability and HA secretion of all 5 NSCLC cell lines except for HA secretion of H460. Emodin had a slight apoptosis induction effect on all cell lines and was not different among cell lines. The knockdown of either the synthases or the receptors blocked emodin effects on viability while the knockdown of HAS2 block emodin effects but not HAS3. Emodin increased cells in the G1/G0 phase, and decreased cells in the S and G2/M phase by down-regulating cyclin A and B and up-regulating cyclin C, D, and E. HAS2 knockdown blocked the effects of emodin on the cell cycle. Conclusions This study demonstrated that emodin regulates the cell cycle of NSCLC cells through the HAS2-HA-CD44/RHAMM interaction-dependent signaling pathway.

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“…Long non-coding ribonucleic acid (LncRNAs) is also involved in the regulation of pyroptosis. Ma et al (81) showed that inhibition of IncRNARP1-85F18.6 could promote the pyroptosis of colorectal cancer cells by modulating the expression level of ΔNp63. In addition, IncRNARP1-85F18.6, ΔNp63, and GSDMD also have certain value in the prognosis and diagnosis of colorectal cancer.…”

Section: Pyroptosis In Cancermentioning

confidence: 99%

Induction of Pyroptosis and Its Implications in Cancer Management

2019

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Pyroptosis is a gasdermins mediated programmed cell death, which has been widely studied in inflammatory disease models. Recently, there are growing evidences that pyroptosis can be chemically induced in cancer cells without any bacterial or viral infection. Pyroptosis may affect all stages of carcinogenesis and has become a new topic in cancer research. In this review, we first briefly introduced pyroptosis. In the subsequent section, we discussed the induction of pyroptosis in cancer and its potential role as a promising target for cancer therapy. In addition, the biological characteristics of gasdermin D (GSDMD) and gasdermin E (GSDME), two important pyroptosis substrates, and their prognostic role in cancer management were reviewed. These results help us to understand the pathogenesis of cancer and develop new drugs, which based on pyroptosis modulation, for cancer patients.

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Biological functions and clinical significance of the newly identified long non‑coding RNA RP1‑85F18.6 in colorectal cancer

Cited by 53 publications

References 38 publications

The role of pyroptosis in cancer: pro-cancer or pro-“host”?

The role of pyroptosis in cancer: pro-cancer or pro-“host”?

Emodin regulates cell cycle of non-small lung cancer (NSCLC) cells through hyaluronan synthase 2 (HA2)-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway

Induction of Pyroptosis and Its Implications in Cancer Management

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