Tumor glycolysis, an essential sweet tooth of tumor cells

Paul, Sumana; Ghosh, Saikat; Kumar, Sushil

doi:10.1016/j.semcancer.2022.09.007

Cited by 124 publications

(63 citation statements)

References 275 publications

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“…Different glycolytic enzymes, such as HK2, PKM2 and LDHA are involved in the progression of cancers [34][35][36]. Pro-oncogenic signaling accelerates the metabolic activities of glycolytic enzymes, mainly by enhancing their expression or post-translational modi cations [37].…”

Section: Discussionmentioning

confidence: 99%

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

wang

Zhao

et al. 2023

Preprint

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Background: Gastric cancer (GC) is one of the most common malignant tumors of the digestive system. As a hallmark of cancer, energy-related metabolic reprogramming was manipulated by various factors, including lncRNAs. It has been shown that lncRNA CCAT1 is a key regulator involved in tumor development. Nevertheless, the exact underlying molecular mechanisms by which lncRNA CCAT1 acts in GC metabolic reprogramming are yet to be elucidated. Methods: The expression of CCAT1 in GC tissues, serum, and exosome that was isolated from plasma and GC cell lines were detected by qRT-PCR. The gain and loss-function assays were performed to explore the role of CCAT1 on GC cells. Xenograft tumor formation models in nude mice were performed to estimate the proliferation of GC cells with CCAT1 stably knocking down in vivo. The proteins interacting with CCAT1 were first analyzed by online databases and further confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assays. The expression of glycolytic signaling pathway-related proteins were probed using western blotting and immunohistochemistry (IHC). Results: In this study, we identified that CCAT1 was remarkably enhanced in the tissues, serum, and plasma exosomes of GC patients as well as in GC cell lines. Functional experiments showed that knockdown of CCAT1 significantly reduced the proliferation, migration and invasion of GC cells in vitro and in vivo, and also decreased glycolytic rate and the expression of glycolytic enzymes in GC cells, whereas overexpression of CCAT1 had opposing effects. Mechanically, CCAT1 interacted with PTBP1 and maintained its stability by inhibiting the ubiquitin-mediated degradation. As a critical splicing factor, PTBP1 induced a switch from PKM1 to PKM2, leading to an increase in the glycolysis of GC cells and ultimately promoting GC progression. Conclusions: Our study exhibited that CCAT1 contributed to GC proliferation, migration and invasion via PTBP1 / glycolysis axis, making it a potential biomarker and therapeutic target in GC patients.

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Section: Discussionmentioning

confidence: 99%

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

wang

Zhao

et al. 2023

Preprint

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“…A direct comparison of Risk-High versus Risk-Low revealed the top 5 enriched signatures in the high-risk group included Glycolysis, mTORC1 signaling, C-MYC target, G2M checkpoint, and E2F targets (Figure 7A). Glycolysis is an essential condition for the occurrence and development of tumors (32). High-risk samples may present a worse prognosis for LUAD patients by upregulating the glycolytic pathway.…”

Section: Pathway Enrichment Analysismentioning

confidence: 99%

By integrating single-cell RNA-seq and bulk RNA-seq in sphingolipid metabolism, CACYBP was identified as a potential therapeutic target in lung adenocarcinoma

et al. 2023

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BackgroundLung adenocarcinoma (LUAD) is a heterogeneous disease with a dismal prognosis for advanced tumors. Immune-associated cells in the microenvironment substantially impact LUAD formation and progression, which has gained increased attention in recent decades. Sphingolipids have a profound impact on tumor formation and immune infiltration. However, few researchers have focused on the utilization of sphingolipid variables in the prediction of LUAD prognosis. The goal of this work was to identify the major sphingolipid-related genes (SRGs) in LUAD and develop a valid prognostic model based on SRGs.MethodsThe most significant genes for sphingolipid metabolism (SM) were identified using the AUCell and WGCNA algorithms in conjunction with single-cell and bulk RNA-seq. LASSO and COX regression analysis was used to develop risk models, and patients were divided into high-and low-risk categories. External nine provided cohorts evaluated the correctness of the models. Differences in immune infiltration, mutation landscape, pathway enrichment, immune checkpoint expression, and immunotherapy were also further investigated in distinct subgroups. Finally, cell function assay was used to verify the role of CACYBP in LUAD cells.ResultsA total of 334 genes were selected as being most linked with SM activity for further investigation, and a risk model consisting of 11 genes was established using lasso and cox regression. According to the median risk value, patients were split into high- and low-risk groups, and the high-risk group had a worse prognosis. The low-risk group had more immune cell infiltration and higher expression of immune checkpoints, which illustrated that the low-risk group was more likely to benefit from immunotherapy. It was verified that CACYBP could increase the ability of LUAD cells to proliferate, invade, and migrate.ConclusionThe eleven-gene signature identified in this research may help physicians create individualized care plans for LUAD patients. CACYBP may be a new therapeutic target for patients with advanced LUAD.

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“…Subsequently, miR-30d induces the downregulation of SLC2A1 and HK1 by directly targeting runt-related transcription factor 1 (RUNX1), which ultimately inhibits the Warburg effect [78]. Numerous studies have demonstrated that the tumor glucose aerobic glycolytic pathway holds great potential as a target for tumor therapy [79,80]. Additionally, it has been revealed that m 6 A methylation plays a significant role in the process of tumor metabolic reprogramming [76,81].…”

Section: A Methylation and Cancer Metabolic Reprogrammingmentioning

confidence: 99%

Roles and implications of mRNA N⁶‐methyladenosine in cancer

Zeng

Huang

Zhang

et al. 2023

Cancer Communications

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RNA N6‐methyladenosine modification is the most prevalent internal modification of eukaryotic RNAs and has emerged as a novel field of RNA epigenetics, garnering increased attention. To date, m6A modification has been shown to impact multiple RNA metabolic processes and play a vital role in numerous biological processes. Recent evidence suggests that aberrant m6A modification is a hallmark of cancer, and it plays a critical role in cancer development and progression through multiple mechanisms. Here, we review the biological functions of mRNA m6A modification in various types of cancers, with a particular focus on metabolic reprogramming, programmed cell death and tumor metastasis. Furthermore, we discuss the potential of targeting m6A modification or its regulatory proteins as a novel approach of cancer therapy and the progress of research on m6A modification in tumor immunity and immunotherapy. Finally, we summarize the development of different m6A detection methods and their advantages and disadvantages.

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Tumor glycolysis, an essential sweet tooth of tumor cells

Cited by 124 publications

References 275 publications

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

By integrating single-cell RNA-seq and bulk RNA-seq in sphingolipid metabolism, CACYBP was identified as a potential therapeutic target in lung adenocarcinoma

Roles and implications of mRNA N⁶‐methyladenosine in cancer

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Tumor glycolysis, an essential sweet tooth of tumor cells

Cited by 124 publications

References 275 publications

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

LncRNA CCAT1 facilitates the progress of gastric cancer via the PTBP1/glycolysis axis

By integrating single-cell RNA-seq and bulk RNA-seq in sphingolipid metabolism, CACYBP was identified as a potential therapeutic target in lung adenocarcinoma

Roles and implications of mRNA N6‐methyladenosine in cancer

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Roles and implications of mRNA N⁶‐methyladenosine in cancer