LncRNA–FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling

Bian, Zehua; Zhang, Jiwei; Li, Min; Feng, Yuyang; Wang, Xue; Zhang, Jia; Yao, Surui; Jin, Guoying; Du, Jie; Han, Wei; Yin, Yuan; Huang, Shenglin; Fei, Bojian; Zou, Jian; Huang, Zhaohui

doi:10.1158/1078-0432.ccr-17-2967

Cited by 246 publications

(229 citation statements)

References 39 publications

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“…Recent evidences have revealed that lncRNAs are frequently deregulated and play vital roles in many human cancers. Our previous studies revealed a variety of CRC related lncRNAs, which are involved in cancer promoting . In addition to these lncRNAs, we also discovered a potential oncogenic lncRNA, SNHG15, in CRC.…”

Section: Discussionmentioning

confidence: 75%

“…Our previous studies revealed a variety of CRC related lncRNAs, which are involved in cancer promoting. [14][15][16][17] In addition to these lncRNAs, we also discovered a potential oncogenic lncRNA, SNHG15, in CRC. SNHG15 was initially found to be overexpressed in GC and could promote cell proliferation and invasion of GC.…”

Section: Discussionmentioning

confidence: 92%

“…[12][13][14] Our previous studies demonstrated that UCA1, LINC00152, FEZF1-AS1, and SNHG6 function as oncogenes to promote cell proliferation, metastasis, and chemoresistance of CRC cells. [15][16][17][18] Small nuclear RNA host gene 15 (SNHG15) is a recently identified lncRNA and locates in chromosome 7p13. Researches showed that SNHG15 is overexpressed in gastric cancer (GC), nonsmall cell lung cancer (NSCLC) and breast cancer, and it could promote cell proliferation in these cancers.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Bian

Jin

et al. 2019

Cancer Medicine

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The incidence and death rate of colorectal cancer ( CRC ) is very high, which brings great need to understand the early molecular events of CRC . These studies demonstrate that long noncoding RNA (lnc RNA ) plays an important role in the occurrence and development of human cancer. Small nucleolar RNA host gene 15 ( SNHG 15) was recently identified as a cancer‐related lnc RNA . In this study, we aimed to evaluate the function and mechanism of SNHG 15 in CRC . The expression of SNHG 15 was detected by quantitative RT ‐ PCR ( qRT ‐ PCR ) in CRC tissues and matched noncancerous tissues ( NCT s). CCK ‐8 assay, colony formation assay, flow cytometric analysis, and nude mouse xenograft mode were used to examine the tumor‐promoting function of SNHG 15 in vitro and in vivo. The binding relationship between SNHG 15, miR‐338‐3p and the target genes of miR‐338‐3p were screened and identified by databases, qRT ‐ PCR , dual luciferase reporter assay and western blot. Our results showed that SNHG 15 was up‐regulated in CRC tissues compared with paired NCT s ( P < 0.0001). High level of SNHG 15 expression predicted poor prognosis of CRC ( P = 0.0051). SNHG 15 overexpression could promote cell proliferation and inhibit cell apoptosis. Animal experiments showed that up‐regulation of SNHG 15 promoted tumor growth in vivo. The results of mechanism experiments showed that SNHG 15 could bind to miR‐338‐3p and block its inhibition on the expression and activity of FOS or RAB 14. In conclusion SNHG 15 promotes cell proliferation through SNHG 15/miR‐338‐3p/ FOS ‐ RAB 14 axis in CRC.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Bian

Jin

et al. 2019

Cancer Medicine

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“…More research is needed to discover and develop effective biomarkers and targets for diagnosis and treatment of CRC. Recently, accumulating evidence has shown that long non-coding RNAs (lncRNAs), non-coding RNA transcripts longer than 200 nucleotides (4), are expressed differentially in various cancers including CRCs, suggesting that lncRNAs have roles in tumorigenesis and tumor metastasis (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation

Zuo

Wang

et al. 2020

Front. Oncol.

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Colorectal cancer (CRC), a common tumor, is characterized by a high mortality rate. Long non-coding RNA maternally expressed gene 3 (MEG3) serves a regulatory role in the carcinogenesis and progression of several types of cancer; however, its role in CRC remains largely unknown. The aim of this study was to explore the regulatory role and mechanism(s) of MEG3 in CRC. The Warburg effect or aerobic glycolysis is characteristic of the metabolism of tumor cells. To determine the effect of MEG3 on glycolysis of CRC cells, we used an XF analyzer to perform glycolysis stress test assays and found that overexpression of MEG3 significantly inhibited glycolysis, glycolytic capacity, as well as lactate production in CRC cells, whereas knockdown of MEG3 produced the opposite effect. Mechanistically, overexpression of MEG3 induced ubiquitin-dependent degradation of c-Myc and inhibited c-Myc target genes involved in the glycolysis pathway such as lactate dehydrogenase A, pyruvate kinase muscle 2, and hexokinase 2. Moreover, we found that MEG3 can be activated by vitamin D and vitamin D receptor (VDR). Clinical data demonstrated that MEG3 was positively associated with serum vitamin D concentrations in patients with CRC. We found that 1,25(OH) 2 D 3 treatment increased MEG3 expression, and knockdown of VDR abolished the effect of MEG3 on glycolysis. These results indicate that vitamin D-activated MEG3 suppresses aerobic glycolysis in CRC cells via degradation of c-Myc. Thus, vitamin D may have therapeutic value in the treatment of CRC.

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“…Emerging evidence has shown the important roles of lncRNAs in cancers, especially their effects on cancer growth and malignant transformation. Dysregulation of some lncRNAs have been reported to regulate important cancer biological processes, such as proliferation (24), metabolism (25), metastasis (26) and cancer cells stemness (15). Recent evidence suggests that lncRNAs can act as ceRNAs to regulate miRNAs, subsequently to regulate expression of target genes.…”

Section: Discussionmentioning

confidence: 99%

lncRNA THAP9-AS1 Promotes Pancreatic Ductal Adenocarcinoma Growth and Leads to a Poor Clinical Outcome via Sponging miR-484 and Interacting with YAP

Yang

Luo

et al. 2020

Clinical Cancer Research

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◥Purpose: Long noncoding RNAs (lncRNA) have been observed in various cancer types. Our bioinformatic analysis of existing databases demonstrated overexpression of lncRNA THAP9-AS1 in pancreatic ductal adenocarcinoma (PDAC). We aimed to investigate the roles and mechanisms of THAP9-AS1 in PDAC.Experimental Design: The overexpression of THAP9-AS1 in samples of patients with pancreatic cancer was characterized and was associated with clinical outcomes. The nonprotein coding property of the THAP9-AS1 was verified. Various in vitro and in vivo experiments were performed to investigate the interaction between THAP9-AS1 and YAP signaling.Results: We demonstrated that lncRNA THAP9-AS1 is overexpressed in PDAC in multiple patient sample sets, which is significantly associated with poor outcome of patients with PDAC. THAP9-AS1 promotes PDAC cells growth both in vitro and in vivo. THAP9-AS1 exerts its effects via enhancing YAP signaling. Ectopic YAP expression overcame the effects of THAP9-AS1 knockdown. Inversely, YAP knockdown diminished the effects of THAP9-AS1 overexpression. THAP9-AS1 acts as a competing endogenous RNA for miR-484, leading to YAP upregulation. Moreover, THAP9-AS1 binds to YAP protein and inhibits the phosphorylation-mediated inactivation of YAP by LATS1. Reciprocally, YAP/TEAD1 complex promotes THAP9-AS1 transcription to form a feed-forward circuit. Importantly, THAP9-AS1 level positively correlates with YAP expression in PDAC tissues. YAP overexpression also predicts a poor outcome in patients with PDAC.Conclusions: Our findings indicate that THAP9-AS1 plays an important role in PDAC growth via enhancing YAP signaling, which in turn also modulates THAP9-AS1 transcription. THAP9-AS1/YAP axis may serve as a potential biomarker and therapeutic target for PDAC treatment.

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LncRNA–FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling

Cited by 246 publications

References 39 publications

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation

lncRNA THAP9-AS1 Promotes Pancreatic Ductal Adenocarcinoma Growth and Leads to a Poor Clinical Outcome via Sponging miR-484 and Interacting with YAP

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