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PIPKIγ promotes tumor growth by facilitating Warburg effect in colorectal cancer

ABSTRACT: Analysis of gene alterations in SW480 cells upon PIPKIγ knockdown. Our findings reveal a new regulatory role of PIPKIγ in Warburg effect and provide a key contributor in colorectal cancer metabolism with potential therapeutic potentials.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130761 | GEO | 2019/05/07

REPOSITORIES: GEO

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PIPKIγ promotes tumor growth by facilitating Warburg effect in colorectal cancer

Project description:PIPKIγ promotes tumor growth by facilitating Warburg effect in colorectal cancer

| PRJNA541292 | ENA

Type I? phosphatidylinositol phosphate kinase promotes tumor growth by facilitating Warburg effect in colorectal cancer.

Project description:BACKGROUND:Emerging evidence suggests that metabolic alterations are a hallmark of cancer cells and contribute to tumor initiation and development. Cancer cells primarily utilize aerobic glycolysis (the Warburg effect) to produce energy and support anabolic growth. The type I? phosphatidylinositol phosphate kinase (PIPKI?) is profoundly implicated in tumorigenesis, however, little is known about its role in reprogrammed energy metabolism. METHODS:Loss- and gain-of-function studies were applied to determine the oncogenic roles of PIPKI? in colorectal cancer. Transcriptome analysis, real-time qPCR, immunohistochemical staining, Western blotting, and metabolic analysis were carried out to uncover the cellular mechanism of PIPKI?. FINDINGS:In this study, we showed that PIPKI? was frequently upregulated in colorectal cancer and predicted a poor prognosis. Genetic silencing of pan-PIPKI? suppressed cell proliferation and aerobic glycolysis of colorectal cancer. In contrast, the opposite effects were observed by overexpression of PIPKI?_i2. Importantly, PIPKI?-induced prolific effect was largely glycolysis-dependent. Mechanistically, PIPKI? facilitated activation of PI3K/Akt/mTOR signaling pathways to upregulate c-Myc and HIF1? levels, which regulate expression of glycolytic enzymes to enhance glycolysis. Moreover, pharmacological inhibition by PIPKI? activity with the specific inhibitor UNC3230 significantly inhibited colorectal cancer glycolysis and tumor growth. INTERPRETATION:Our findings reveal a new regulatory role of PIPKI? in Warburg effect and provide a key contributor in colorectal cancer metabolism with potential therapeutic potentials. FUND: National Key Research and Development Program of China, Outstanding Clinical Discipline Project of Shanghai Pudong, Natural Science Foundation of China, and Science and Technology Commission of Shanghai Municipality.

| S-EPMC6604371 | biostudies-literature

Expression analysis of colorectal cancer cell line SW480 expressing FOXC2

Project description:Investigation of whole genome gene expression level changes in a colorectal cancer cell line SW480 expressing FOXC2, compared to the pBabe control cells. Genes associated with metastasis regulated by FOXC2 in colorectal cancer were analysed. The role of FOXC2 in breast cancer metastasis are further described in Mani SA, Yang J et al. Mesenchyme Forkhead 1 (FOXC2) plays a key role in metastasis and is associated with aggressive basal-like breast cancers. PNAS 2007; 104: 10069-10074 . A six chip study using total RNA recovered from three separate cultures of SW480/pBabe and three separate cultures of SW480/FOXC2. Each chip measures the expression level of 45033 genes from SW480/pBabe or SW480/FOXC2.

2014-07-02 | E-GEOD-58980 | biostudies-arrayexpress

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Project description:Two isogenic human colorectal cancer cell lines (primary SW480 cell line and its lymph node metastatic variant SW620 cell line),as an in vitro metastatic model. We have demonstrated that SW620 cell line possesses high metastasis potential and SW480 cell linepossesses low metastatic potential. We want to compare the whole cell microRNAs profiles of two isogenic colorectal cancer cell lines (SW480 and SW620 cell line), to gain an insight into the molecular events of colon cancer metastasis.

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Colorectal cancer cell lines basal expression [microarray]

Project description:We performed microarray analysis of four colorectal cancer cell lines (Caco2, HCT116, SW480, and SW620).

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miRNAs in colorectal cancer metastasis

Project description:Metastasis is a complex process involving multiple steps. We were interested in the role of microRNAs (miRNAs) in the process of liver colonization by colorectal cancer cells. We hypothesized that the comparison between non-metastatic versus metastatic isogenic cell line should thus offer valuable insight to the molecular mechanisms involved in developing metastatic behavior. KM12C/KM12SM and SW480/SW620 are probably the best available models of isogenic cell lines differing in metastatic properties for colorectal cancer. Our first goal was to identify miRNAs that contribute to the metastatic traits of the isogenic colorectal cancer cell lines, KM12C/KM12SM and SW480/SW620. Total RNA was extracted from cells using the mirVana kit (Ambion). Total RNA (1 µg) from KM12C and SW480 (poorly metastatic) and KM12SM and SW620 (highly metastatic) cells was used to analyze the global miRNA expression profiling with TaqMan Megaplex human array A (v2.0) and B (v3.0) (Applied Biosystems).

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MNX1-AS1, a c-Myc induced lncRNA, promotes the Warburg effect by regulating PKM2 nuclear translocation

Project description:Altered glycolysis is the most fundamental metabolic change associated with the Warburg effect. However, the precise mechanisms are not completely understood. Here we dissect how MNX1-AS1 reinforces the Warburg effect through facilitating the non-glycolytic actions of PKM2 in the nucleus. We found that MNX1-AS1 expression was frequently overexpressed in hepatocellular carcinoma (HCC). In the context of HCC, we show MNX1-AS1 acts as a scaffold to promote interactions between PKM2 and importin α5. Upon EGFR activation, the resulting ternary complex drives the translocation of PKM2 into the nucleus. In consequence, glycolytic pathway components including key mediators of the Warburg effect (LDHA, Glut1 and PDK1) are upregulated. Manipulating MNX1-AS1 elicited robust effects on glycolysis associated with marked changes in HCC growth in vitro and in vivo, indicative of the significant contribution of MNX1-AS1 to tumorigenesis. Moreover, while MNX1-AS1 expression is driven by c-Myc, its actions associated with PKM2 were shown to be downstream and independent of c-Myc. Given the status of MNX1-AS1 as a pan-cancer upregulated lncRNA, this implicitly highlights the potential of targeting MNX1-AS1 to selectively counter the Warburg effect in a range of tumor types.

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