&lt;p&gt;LncRNA PTTG3P Sponge Absorbs microRNA-155-5P to Promote Metastasis of Colorectal Cancer&lt;/p&gt;

Liu, Ning; Dou, Lei; Zhang, Xinxin

doi:10.2147/ott.s248457

Cited by 16 publications

(12 citation statements)

References 20 publications

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“…These results con rmed that PTTG3P overexpression serves as a valuable prognostic biomarker and aids innovatively e cient therapies for CRC patients. Additionally, our ndings stands in line with other research, Liu,et al [16] reported that PTTG3P was remarkably upregulated in CRC tumor samples than that in normal samples. Zhou, et al [17] revealed that PTTG3P is a valuable resource for identi cation in HCC progression and is useful for biomarker development.…”

Section: Discussionsupporting

confidence: 93%

WITHDRAWN: N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Progression via IGF2BP2

Zheng

Xie

et al. 2021

Preprint

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Background N6-methyladenosine (m6A) and long noncoding RNAs (lncRNAs) emerged as crucial players in colorectal cancer (CRC) progression, but the m6A modified lncRNA PTTG3P in CRC are still need to be systematically defined. Methods qRT-PCR was adopted to measure the PTTG3P expression. Survival analysis was used to explore the correlation between the expression of PTTG3P and CRC patients prognosis. Receiver operating curve (ROC) was tested to evaluate the PTTG3P predictive ability. Functional studies were examined by CCK-8, glucose uptake, lactate assay, ATP assay, ECAR assay and xenograft mice model. Mechanistic studies were explored by GSEA, methylated RNA immunoprecipitation sequencing (MeRIP-Seq) and RNA immunoprecipitation (RIP).Results PTTG3P was upregulated in CRC and closely related to poor prognosis. Through gain and loss of function approaches, PTTG3P facilitated proliferation and glycolysis through Hippo pathway, and glycolysis inhibitor (2-DG ,3-BG) and LDHA knockdown could rescue cell proliferation. Mechanically, m6A methylation induced the elevation of PTTG3P by increasing its stability , and insulin like growth factor-2 mRNA binding proteins 2 (IGF2BP2) involved in the progression. Finally, rescue assays validated the effect of METTL3/PTTG3P/YAP1 axis in CRC progression. Conclusions m6A-induced PTTG3P could facilitates CRC development via interacting with IGF2BP2, which provides a predictive biomarker and theraperutic target for CRC.

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Section: Discussionsupporting

confidence: 93%

WITHDRAWN: N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Progression via IGF2BP2

Zheng

Xie

et al. 2021

Preprint

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“…These results con rmed that PTTG3P serves as a valuable prognostic biomarker and aids innovatively e cient therapies for CRC patients. Additionally, our ndings stand in line with other research, Liu, et al [10] reported that PTTG3P was remarkably upregulated in CRC tumor samples than that in normal samples. Zhou, et al [11] revealed that PTTG3P is a valuable resource for identi cation in HCC progression and is useful for biomarker development.…”

Section: Discussionsupporting

confidence: 93%

WITHDRAWN: A Novel Axis HIF1A/miR-1271-5p/lncRNA PTTG3P/YAP1 Contributes to Colorectal Cancer Progression and Relates to an Immune-Suppressing Microenvironment

Yang¹,

Zhang²,

liu³

et al. 2021

Preprint

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Background Pseudogene has emerged as key regulators of important biological processes involved in human cancers. However, the PTTG3P biological function in colorectal cancer (CRC) needs further to be clarified. Methods qRT-PCR was adopted to measure the PTTG3P expression in different cell line and CRC tissues. Cellular localization of PTTG3P was detected by subcellular fractionation assay. In vitro and in vivo experiments were carried out to explore the bioeffect of PTTG3P in CRC cells. Chromatin immunoprecipitation (ChIP), luciferase assay and RIP were explored to certify the direct binding of PTTG3P and microRNA. Results PTTG3P was upregulated in CRC and closely related to poor prognosis. Through gain and loss of function approaches, PTTG3P facilitated proliferation and glycolysis through YAP1, and glycolysis inhibitor (2-DG,3-BG) and LDHA knockdown could rescue cell proliferation and tumorigenesis. Mechanically, miR-1271-5p modulates PTTG3P expression and miR-1271-5p mimics could recover the PTTG3P function. Also HIF1A increased PTTG3P expression in both normoxia and hypoxia conditions by ameliorating miR-1271-5p expression. In addition, silencing PTTG3P decreases the level of inflammatory cytokines TNF-α, IL-1β and IL-6, and low PTTG3P expression relates with CD8+ T, NK and TFH cells infiltration. Conclusions Our findings verified the oncogenic function of PTTG3P in assisting the cell proliferation and glycolysis, demonstrating the pivotal roles of HIF1A/miR-1271-5p/lncRNA PTTG3P/YAP1 in CRC progression, which proposes a novel approach for clinical treatment.

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“…Additionally, our findings stand in line with other research, Liu, et al [13] reported that PTTG3P was remarkably upregulated in CRC tumor samples than that in normal samples. Zhou, et al [14] revealed that PTTG3P is a valuable resource for identification in HCC progression and is useful for biomarker development.…”

Section: Discussionsupporting

confidence: 93%

WITHDRAWN: A FoxM1/lncRNA PTTG3P/YAP1 Positive Feedback Loop Controls Colorectal Cancer Progression

Zheng

Liu

et al. 2021

Preprint

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Background Pseudogenes are vital regulators of cancer progression. PTTG3P biological function in colorectal cancer (CRC) needs further to be clarified. Methods qRT-PCR was adopted to measure the PTTG3P expression. Functional studies were examined by CCK-8, glucose uptake, lactate assay, ATP assay, ECAR assay and xenograft mice model. The mechanism of PTTG3P was carried by GSEA. Chromatin immunoprecipitation (ChIP) and luciferase assay were explored to certify the binding activity between PTTG3P promoter region and FoxM1. Results Ectopic expression of PTTG3P was involved in CRC and related to dismal prognosis. Experimental evidence discovered that PTTG3P enhanced cell proliferation and glycolysis through YAP1 and regulated FoxM1(Hippo pathway target gene). Further, LDHA knockdown or glycolysis inhibitor (2-DG,3-BG) recovered PTTG3P-induced proliferation. Mechanically, FoxM1 increase PTTG3P expression at transcription level and the PTTG3P promoter region of -900 to -1200 nt is necessary for binding with FoxM1, thus forming a positive feedback loop to facilitates the CRC progression. Additionally, FoxM1 depletion could rescue the PTTG3P function. Conclusions A FoxM1/lncRNA PTTG3P/YAP1 positive feedback loop plays a vital part in CRC progression, and targeting FoxM1, PTTG3P and YAP1 provides therapeutic targets for CRC treatment.

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<p>LncRNA PTTG3P Sponge Absorbs microRNA-155-5P to Promote Metastasis of Colorectal Cancer</p>

Cited by 16 publications

References 20 publications

WITHDRAWN: N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Progression via IGF2BP2

WITHDRAWN: N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Progression via IGF2BP2

WITHDRAWN: A Novel Axis HIF1A/miR-1271-5p/lncRNA PTTG3P/YAP1 Contributes to Colorectal Cancer Progression and Relates to an Immune-Suppressing Microenvironment

WITHDRAWN: A FoxM1/lncRNA PTTG3P/YAP1 Positive Feedback Loop Controls Colorectal Cancer Progression

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