LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma

Yang, Xiangchou; Ye, Haihao; He, Min; Zhou, Xiaohai; Sun, Nana; Guo, Weidong; Lin, Xiaoji; Huang, He; Yao, Rongxin; Wang, Hong

doi:10.1016/j.bbrc.2018.02.211

Cited by 70 publications

(57 citation statements)

References 25 publications

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“…Li et al found that lncRNA SNHG3 correlates to energy metabolism by regulating miRNAs and EIF4AIII to regulate glycolysis, Kreb's cycle, and oxidative phosphorylation pathways. As for c‐Myc regulation, CCAT1‐L, GHET1, and PDIA3P were critically involved in modulating transcription and RNA stability of c‐Myc . We have added another layer of complexity in which LINC00504 functions as a coactivator of c‐Myc to reprogram metabolic pathways.…”

Section: Discussionmentioning

confidence: 99%

A noncoding RNA LINC00504 interacts with c‐Myc to regulate tumor metabolism in colon cancer

Feng

Liu

et al. 2019

J of Cellular Biochemistry

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Accumulating evidence has shown a critical role of long‐non‐coding RNAs (lncRNAs) during multiple tumor progression. However, the potential functions of LINC00504 in colon cancer as well as its mechanisms remain obscure. By lncRNA profiling, we identified LINC00504 as a novel oncogenic lncRNA in colon cancer. The lncRNA LINC00504 was markedly upregulated in colon cancer cell lines and specimens. LINC00504 increases viability and migration of colon cells in vitro. Furthermore, LINC00504 also enhances colon cancer xenograft tumors in vivo. We noted that LINC00504 regulates metabolism at a transcriptional level which influences multiple metabolic pathways, such as glucose metabolism, pentose phosphate pathway, and tricarboxylic acid cycle. Mechanistic study showed that LINC00504 could interact with c‐Myc to promote chromatin recruitment of c‐Myc and enhance its transactivation activity. Collectively, our results showed that LINC00504 serves as an important transcriptional regulator for c‐Myc in colon cancer cells. LINC00504 can reprogram central metabolism in colon cancer cells implying that LINC00504 may serve as a potential target for therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

A noncoding RNA LINC00504 interacts with c‐Myc to regulate tumor metabolism in colon cancer

Feng

Liu

et al. 2019

J of Cellular Biochemistry

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“…G6PD expression is transcriptionally activated by c-Myc, which is further enhanced by lncRNA protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P) via interacting with c-Myc. Thus, PDIA3P promotes PPP and enables multiple myeloma progression [90]. Another study showed that lncRNA prostate cancer gene expression marker 1 (PCGEM1) binds to target promoters through interacting with c-Myc and increasing its chromatin recruitment, thus enhances c-Myc transactivation activity and affects multiple metabolism pathways including PPP [61].…”

Section: Lncrnas Regulate Glucose Metabolismmentioning

confidence: 99%

LncRNAs regulate metabolism in cancer

et al. 2020

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Metabolic reprogramming is a hallmark of cancer. Mammalian genome is characterized by pervasive transcription, generating abundant non-coding RNAs (ncRNAs). Long non-coding RNAs (lncRNAs) are freshly discovered functional ncRNAs exerting extensive regulatory impact through diverse mechanisms. Emerging studies have revealed widespread roles of lncRNAs in the regulation of various cellular activities, including metabolic pathways. In this review, we summarize the latest advances regarding the regulatory roles of lncRNAs in cancer metabolism, particularly their roles in mitochondrial function, glucose, glutamine, and lipid metabolism. Moreover, we discuss the clinical application and challenges of targeting lncRNAs in cancer metabolism. Understanding the complex and special behavior of lncRNAs will allow a better depiction of cancer metabolic networks and permit the development of lncRNA-based clinical therapies by targeting cancer metabolism.

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“…p53 is the main adverse regulator during tumor metabolic reprogramming (15). p53 inhibits glycolysis by inducing glycolysis and apoptosis regulator (TIGAR), inhibiting phosphoglycerate mutase (PGM) to upregulate expression of TP53, and repressing glucose transporter (GLUT)-1 and GLUT -4 (6,(16)(17)(18). Also, p53 can alter oxygen consumption and the synthesis of cytochrome c oxidase 2 (SCO2) protein, which is critical for regulating the cytochrome c oxidase(COX) complex (19).…”

Section: Glucose Metabolism and The Warburg Effect In Tumorsmentioning

confidence: 99%

Glucose Metabolism on Tumor Plasticity, Diagnosis, and Treatment

et al. 2020

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Malignant cells support tumor proliferation and progression by adopting to metabolic changes. Tumor cells altered metabolism by increasing glucose uptake and fermentation of glucose to lactate, even in the aerobic state and the presence of functioning mitochondria. Glucose metabolism in tumor plasticity has attracted great interests by clinicians and scientists in the past decades. This review discusses the previous and emerging researches on the tumor plasticity altered by changing glucose metabolism in different cancer cells, including cancer stem cells (CSCs). In addition, we summarize the rising applications of glucose metabolism in tumor diagnosis and treatment. Our objective is to direct future investigation on this altered metabolic phenotype and its application in patient care.

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LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma

Cited by 70 publications

References 25 publications

A noncoding RNA LINC00504 interacts with c‐Myc to regulate tumor metabolism in colon cancer

A noncoding RNA LINC00504 interacts with c‐Myc to regulate tumor metabolism in colon cancer

LncRNAs regulate metabolism in cancer

Glucose Metabolism on Tumor Plasticity, Diagnosis, and Treatment

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