Cucurbitacin B suppresses proliferation of pancreatic cancer cells by ceRNA: Effect of miR‐146b‐5p and lncRNA‐AFAP1‐AS1

Zhou, Jingkai; Liu, Mei; Chen, Yanan; Xu, Shoufang; Guo, Yingjie; Zhao, Limei

doi:10.1002/jcp.27264

Cited by 32 publications

(10 citation statements)

References 48 publications

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“…There has been considerable progress in the study of ceRNAs in PC. For example, lncRNA-PVT1 promotes PC cell proliferation and migration by sponging miR-448 [24]; cucurbitacin B inhibits PC cell proliferation both in vitro and in vivo through lncRNA-AFAP1-AS1 binding with miR-146b-5p [25]; and PXN-AS1 acts as a ceRNA of miR-3064, which upregulates PIP4K2B expression and suppresses the progression of pancreatic cancer [26]. In our research, subcellular fractionation assays indicated that LINC00514 was mostly located in the cytoplasm, which provided a basis for LINC00514 to act as a ceRNA in the initiation and progression of PC.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression

Han

Xiong

et al. 2020

J Exp Clin Cancer Res

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Background: Pancreatic cancer (PC) is one of the most aggressive cancers and has an extremely poor prognosis worldwide. Long noncoding RNA (lncRNA) has been reported to be a potential prognostic biomarker in the initiation and prognosis of PC. Nevertheless, the biological functions and the detailed molecular mechanism of LINC00514 in PC remain unclear. Methods: We measured the expression level of LINC00514 in PC tissues and cell lines by quantitative real-time PCR. Gain-and loss-of-function experiments were performed to explore the bioeffects of LINC00514 on PC development both in vitro and in vivo. Subcellular fractionation, luciferase reporter assay, RNA immunoprecipitation assay, pulldown assay and western blotting were performed to investigate the oncogenic molecular mechanisms of LINC00514. Results: In this study, LINC00514 was shown to be upregulated in PC tissues and cell lines. Increased LINC00514 expression was significantly associated with the clinical progression and prognosis of PC patients. In addition, silencing LINC00514 inhibited PC cell proliferation, migration and invasion, while LINC00514 overexpression promoted these processes. Moreover, LINC00514 knockdown remarkably inhibited PC development and metastasis in vivo. Deeper investigations indicated that LINC00514 acted as a sponge for microRNA-28-5p (miR-28-5p) in PC and that Rap1b was a downstream target of miR-28-5p. Furthermore, the positive correlation of LINC00514 and Rap1b and the negative correlation between miR-28-5p and LINC00514 (or Rap1b) were revealed. Based on the rescue assays, Rap1b inhibition partially suppressed the oncogenic effect of LINC00514 overexpression on PC cell proliferation, migration and invasion. Conclusions: This study is the first to characterize the oncogenic function of the long noncoding RNA LINC00514 in pancreatic cancer progression by acting as a competing endogenous RNA (ceRNA) of miR-28-5p to upregulate Rap1b expression. Understanding this molecular mechanism might contribute to further discoveries of better diagnostic and therapeutic options for pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression

Han

Xiong

et al. 2020

J Exp Clin Cancer Res

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“…Cucurbitacins and their derivatives have various biological and pharmacological actions, including anticancer effects [166,167]. Cucurbitacin B (Figure 3) demonstrated anti-STAT3 effects in human pancreatic cancer cells [168,169] and leukemia cells [170] ( Table 2). Even though cucurbitacin E decreased the amount of phosphorylated STAT3 in human bladder cancer cells, it did not alter the levels of STAT3 [171].…”

Section: Cucurbitacinsmentioning

confidence: 99%

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

Bose¹,

Banerjee²,

Mondal³

et al. 2020

Cells

145

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Cancer is a prevalent cause of mortality around the world. Aberrated activation of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway promotes tumorigenesis. Natural agents, including phytochemicals, exhibit potent anticancer activities via various mechanisms. However, the therapeutic potency of phytoconstituents as inhibitors of JAK/STAT signaling against cancer has only come into focus in recent days. The current review highlights phytochemicals that can suppress the JAK/STAT pathway in order to impede cancer cell growth. Various databases, such as PubMed, ScienceDirect, Web of Science, SpringerLink, Scopus, and Google Scholar, were searched using relevant keywords. Once the authors were in agreement regarding the suitability of a study, a full-length form of the relevant article was obtained, and the information was gathered and cited. All the complete articles that were incorporated after the literature collection rejection criteria were applied were perused in-depth and material was extracted based on the importance, relevance, and advancement of the apprehending of the JAK/STAT pathway and their relation to phytochemicals. Based on the critical and comprehensive analysis of literature presented in this review, phytochemicals from diverse plant origins exert therapeutic and cancer preventive effects, at least in part, through regulation of the JAK/STAT pathway. Nevertheless, more preclinical and clinical research is necessary to completely comprehend the capability of modulating JAK/STAT signaling to achieve efficient cancer control and treatment.

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“…LncRNAs also play roles in the development of PC as competitive endogenous RNAs (ceRNAs) [46,47]. CeRNA is a special manifestation of lncRNA, which can competitively combine with corresponding miRNAs, inhibit the activity of miRNAs, regulate the expression of downstream targeted genes, and thus regulating intracellular pathophysiological changes [48]. Studies have found that lncRNA PVT1 and miR-488 can promote the growth and invasion of PC by regulating ceRNA [36].…”

Section: Discussionmentioning

confidence: 99%

Silencing of FTX suppresses pancreatic cancer cell proliferation and invasion by upregulating miR-513b-5p

Zhang

Liu

et al. 2021

BMC Cancer

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Background Abnormal expression of long non-coding RNA (lncRNA) FTX (five prime to Xist), which is involved in X chromosome inactivation, has been reported in various tumors. However, the effect of FTX on the development of pancreatic cancer (PC) has not been elucidated. The purpose of this study was to explore the possible molecular mechanism of FTX in PC. Methods Quantitative real-time PCR (qRT-PCR) was used to measure the expression levels of FTX and miR-513b-5p in PC cell lines. Proliferation and apoptosis of PC cells were determined by CCK-8, Edu assay, and flow cytometry. Invasion and migration ability of PC cells were detected by Transwell assay and scratch test. Bioinformatics analysis, luciferase reporter gene assay, and RNA immunoprecipitation (RIP) assay were used to verify the direct binding between FTX and miR-513b-5p. The xenotransplantation mouse model was established to explore the effect of FTX and miR-513b-5p on the PC tumor growth in vivo. Results The expression levels of FTX were increased in PC cell lines, and silencing of FTX remarkably suppressed the invasion ability and cell viability. Besides, FTX could bind to miR-513b-5p as a competitive endogenous RNA, thus promoting the invasion and proliferation ability of PC cells. Moreover, knockdown of FTX inhibited the tumor growth and increased the expression levels of miR-513b-5p and apoptosis-related proteins in vivo. Conclusions FTX could directly combine with miR-513b-5p as a competitive endogenous RNA, thus promoting the occurrence and development of PC in vitro and in vivo.

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Cucurbitacin B suppresses proliferation of pancreatic cancer cells by ceRNA: Effect of miR‐146b‐5p and lncRNA‐AFAP1‐AS1

Cited by 32 publications

References 48 publications

Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression

Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

Silencing of FTX suppresses pancreatic cancer cell proliferation and invasion by upregulating miR-513b-5p

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