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

Zuo, Siyu; Wu, Lei; Wang, Yi; Yuan, Xiaoqin

doi:10.3389/fonc.2020.00274

Cited by 51 publications

(42 citation statements)

References 62 publications

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“…( 193,195,196 ) In several studies, this decrease in glycolysis is linked to inhibition of c‐Myc, a regulator of glycolytic gene transcription, by 1,25D. ( 192,195,196 ) It has also been reported that 1,25D is able to suppress glutamine metabolism in breast cancer cells, partially through inhibiting transcription of the glutamine transporter. ( 197 ) In skin, vitamin D can also protect against cancer by increasing glycolysis, autophagy, and mitophagy after UV‐mediated DNA damage to maintain DNA repair in keratinocytes.…”

Section: Effects Of 125d On T‐cell Metabolismmentioning

confidence: 99%

“…Vitamin D is suppressive of glycolysis in multiple cancers. (192)(193)(194)(195) For highly glycolytic cancer cells, this inhibition of glucose metabolism is detrimental, resulting in loss of proliferation and increased apoptosis. (193,195,196) In several studies, this decrease in glycolysis is linked to inhibition of c-Myc, a regulator of glycolytic gene transcription, by 1,25D.…”

Section: Cellular Metabolismmentioning

confidence: 99%

“…(192)(193)(194)(195) For highly glycolytic cancer cells, this inhibition of glucose metabolism is detrimental, resulting in loss of proliferation and increased apoptosis. (193,195,196) In several studies, this decrease in glycolysis is linked to inhibition of c-Myc, a regulator of glycolytic gene transcription, by 1,25D. (192,195,196) It has also been reported that 1,25D is able to suppress glutamine metabolism in breast cancer cells, partially through inhibiting transcription of the glutamine transporter.…”

Section: Cellular Metabolismmentioning

confidence: 99%

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Vitamin D and Immune Regulation: Antibacterial, Antiviral, Anti‐Inflammatory

et al. 2020

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Regulation of immune function continues to be one of the most well-recognized extraskeletal actions of vitamin D. This stemmed initially from the discovery that antigen presenting cells such as macrophages could actively metabolize precursor 25-hydroxyvitamin D (25D) to active 1,25-dihydroxyvitamin D (1,25D). Parallel observation that activated cells from the immune system expressed the intracellular vitamin D receptor (VDR) for 1,25D suggested a potential role for vitamin D as a localized endogenous modulator of immune function. Subsequent studies have expanded our understanding of how vitamin D exerts effects on both the innate and adaptive arms of the immune system. At an innate level, intracrine synthesis of 1,25D by macrophages and dendritic cells stimulates expression of antimicrobial proteins such as cathelicidin, as well as lowering intracellular iron concentrations via suppression of hepcidin. By potently enhancing autophagy, 1,25D may also play an important role in combatting intracellular pathogens such as M. tuberculosis and viral infections. Local synthesis of 1,25D by macrophages and dendritic cells also appears to play a pivotal role in mediating T-cell responses to vitamin D, leading to suppression of inflammatory T helper (Th)1 and Th17 cells, and concomitant induction of immunotolerogenic Tregulatory responses. The aim of this review is to provide an update on our current understanding of these prominent immune actions of vitamin D, as well as highlighting new, less well-recognized immune effects of vitamin D. The review also aims to place this mechanistic basis for the link between vitamin D and immunity with studies in vivo that have explored a role for vitamin D supplementation as a strategy for improved immune health. This has gained prominence in recent months with the global coronavirus disease 2019 health crisis and highlights important new objectives for future studies of vitamin D and immune function.

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Section: Effects Of 125d On T‐cell Metabolismmentioning

confidence: 99%

Section: Cellular Metabolismmentioning

confidence: 99%

Section: Cellular Metabolismmentioning

confidence: 99%

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Vitamin D and Immune Regulation: Antibacterial, Antiviral, Anti‐Inflammatory

et al. 2020

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“…In CC, MEG3 had been illustrated to be implicated in malignant cell functions [32], glycolysis [35], and chemoresistance [34] of CC cells. Next, we verified an anti-tumor role of MEG3 in CC cells by inhibiting cell viability, colony formation ability, cell cycle progression and invasion, and promoting ER stress.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway

Huang¹,

Xie²,

Cheng³

et al. 2021

neo

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LncRNA maternally expressed gene 3 (MEG3) is a potential prognostic and diagnostic biomarker in colorectal carcinoma (CC). However, its cellular functions and mechanism remain not fully uncovered. Relative expression of MEG3, miRNA (miR)-103a-3p, and pyruvate dehydrogenase E1 subunit beta (PDHB) was detected by RT-qPCR and western blotting. Cell proliferation was measured by CCK-8 assay, colony formation assay, and flow cytometry, as well as xenograft tumor assay. Transwell assay examined cell invasion. Endoplasmic reticulum (ER) stress was eva luated by western blotting. Dual-luciferase reporter assay and RNA immunoprecipitation determined the relationship between miR-103a-3p and MEG3 or PDHB. Expression of MEG3 was downregulated in human CC tumor tissues and cells (SW620 and HCT116), accompanied by higher miR-103a-3p and lower PDHB. Restoring MEG3 suppressed cell viability, colony formation ability, and invasion, 2 arrested cell cycle, and induced apoptosis rate in SW620 and HCT116 cells, as well as promoted expression of ER stress-related proteins (GRP78, ATF6, CHOP, caspase-3, and caspase-9). Furthermore, MEG3 overexpression hindered tumor growth and facilitated ER stress in vivo. Molecularly, miR-103a-3p was a target of MEG3, and further targeted PDHB. Similarly, in function, blocking miR-103a-3p suppressed CC in vitro by affecting proliferation, invasion, and ER stress; in addition, restoring miR-103a-3p partially counteracted the suppressive role of MEG3 in CC cells. MEG3 sponged miR-103a-3p to suppress CC malignancy by inducing ER stress and inhibiting cell proliferation and invasion via upregulating PDHB, suggesting a novel MEG3/miR-103a-3p/PDHB ceRNA pathway. Key words : MEG3; ER stress; miR-103a-3p; pyruvate dehydrogenase E1 subunit beta (PDHB); colorectal carcinoma Endoplasmic reticulum (ER) stress, caused by the accumulation of unfolded or misfolded proteins, plays a dual role in tumorigenesis and development [1], by linking to fundamental biological processes, such as proliferation, apoptosis, migration, invasion and autophagy [2-4]. In response to ER stress, unfolded protein response (UPR) is activated to promote tumor-survival response or anti-tumor response [5, 6]. Not surprisingly, ER stress and UPR are associated with intestinal diseases, including colorectal carcinoma (CC) [7, 8]. CC is the third most common cancer according to global cancer statistics 2018 of the International Agency for Research on Cancer [9], and its incidence and mortality are expected to be rapidly increasing in many low-income and middle-income countries [10]. The survival of CC patients is closely related to the stage of CC [11], thus it is essential to identify more efficient mole cular targets for better understanding of the mechanism underlying CC progression, as well as seeking early diagnostic markers. Recently, it has been well-documented that long noncoding RNAs (lncRNAs) as key regulators mediate competing endogenous RNA (ceRNA) network to regulate carcinogenesis, progression and treatment of CC [12, 13]. LncRNA...

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“…12,13 For instance, lncRNA maternally expressed gene 3 (MEG3) suppressed proliferation and invasion via regulation of glycolysis in colorectal cancer. 14 Similarly, the curcumin analogue WZ35 inhibited glycolysis and facilitated the generation of reactive oxygen species (ROS), promoting JNK-dependent apoptosis of gastric cancer cells. 15 Xi et al 16 also reported that human equilibrative nucleoside transporter 1 (hENT1) was involved in modulating chemotherapy sensitivity of pancreatic cancer cells by inhibiting glycolysis.…”

Section: Introductionmentioning

confidence: 99%

<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

Han¹,

Shi²,

Cao³

et al. 2020

OTT

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Glioma is the most common type of intracranial malignant tumor, with a great recurrence rate due to its infiltrative growth, treatment resistance, intra-and intertumoral genetic heterogeneity. Recently, accumulating studies have illustrated that activated aerobic glycolysis participated in various cellular and clinical activities of glioma, thus influencing the efficacy of radiotherapy and chemotherapy. However, the glycolytic process is too complicated and ambiguous to serve as a novel therapy for glioma. In this review, we generalized the implication of key enzymes, glucose transporters (GLUTs), signalings and transcription factors in the glycolytic process of glioma. In addition, we summarized therapeutic interventions via the above aspects and discussed promising clinical applications for glioma.

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

Cited by 51 publications

References 62 publications

Vitamin D and Immune Regulation: Antibacterial, Antiviral, Anti‐Inflammatory

Vitamin D and Immune Regulation: Antibacterial, Antiviral, Anti‐Inflammatory

LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway

<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

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