LINC01615 maintains cell survival in adaptation to nutrient starvation through the pentose phosphate pathway and modulates chemosensitivity in colorectal cancer

Zhang, Yi; Liu, Xu; Ren, Zeqiang; Liu, Xin; Song, Jun; Zhang, Chong; Gong, Shuai; Wu, Nai; Zhang, Xiuzhong; Xie, Chanbin; Lu, Zhixing; Ma, Min; Chen, Yifei; Lin, Changwei

doi:10.1007/s00018-022-04675-7

Cited by 15 publications

(13 citation statements)

References 58 publications

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“…Mechanistically, the process of serum starvation led to the degradation of METTL3, consequently leading to an elevation in the stability and expression level of LINC01615. LINC01615 was found to enhance the expression of G6PD, an essential enzyme in the PPP, through its competitive binding with hnRNPA1 and its facilitation of pro‐G6PD mRNA splicing 118 . In addition, the expression of lncRNA LBX2‐AS1 level was upregulated in CRC tissues, and this upregulation was observed to be positively associated with 5‐FU resistance.…”

Section: Interaction Between M6a Modification and Lncrna In Cancer Dr...mentioning

confidence: 95%

“…LINC01615 was found to enhance the expression of G6PD, an essential enzyme in the PPP, through its competitive binding with hnRNPA1 and its facilitation of pro‐G6PD mRNA splicing. 118 In addition, the expression of lncRNA LBX2‐AS1 level was upregulated in CRC tissues, and this upregulation was observed to be positively associated with 5‐FU resistance. Mechanistic investigations suggested that METTL3‐mediated m6A modification increased the stability and expression level of LBX2‐AS1.…”

Section: Interaction Between M6a Modification and Lncrna In Cancer Dr...mentioning

confidence: 97%

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New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

Jin,

Fan

2023

Cell Proliferation

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Drug resistance is perhaps the greatest obstacle in improving outcomes for cancer patients, leading to recurrence, progression and metastasis of various cancers. Exploring the underlying mechanism worth further study. N6‐methyladenosine (m6A) is the most common RNA modification found in eukaryotes, playing a vital role in RNA translation, transportation, stability, degradation, splicing and processing. Long noncoding RNA (lncRNA) refers to a group of transcripts that are longer than 200 nucleotides (nt) and typically lack the ability to code for proteins. LncRNA has been identified to play a significant role in regulating multiple aspects of tumour development and progression, including proliferation, metastasis, metabolism, and resistance to treatment. In recent years, a growing body of evidence has emerged, highlighting the crucial role of the interplay between m6A modification and lncRNA in determining the sensitivity of cancer cells to chemotherapeutic agents. In this review, we focus on the recent advancements in the interaction between m6A modification and lncRNA in the modulation of cancer drug resistance. Additionally, we aim to explore the underlying mechanisms involved in this process. The objective of this review is to provide valuable insights and suggest potential future directions for the reversal of chemoresistance in cancer.

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Section: Interaction Between M6a Modification and Lncrna In Cancer Dr...mentioning

confidence: 95%

Section: Interaction Between M6a Modification and Lncrna In Cancer Dr...mentioning

confidence: 97%

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

Jin,

Fan

2023

Cell Proliferation

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“…Zhang et al demonstrated that starvation degraded METTL3 through the autophagy-lysosome pathway. More critically, starvation-reduced METTL3 was also reported to upregulate LINC01615 in an m6A modification-dependent manner and then to maintain CRC cell survival (30). A previous study has suggested that METTL3 was SUMOylated by SUMO1, which is responsible for the accumulation of METTL3 in CRC cells (57).…”

Section: Effects Of Mettl3 On Crcmentioning

confidence: 99%

m6A modification on the fate of colorectal cancer: functions and mechanisms of cell proliferation and tumorigenesis

et al. 2023

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N6-methyladenosine (m6A) is the most pervasive RNA modification in eukaryotic cells. The dynamic and reversible m6A modification of RNA plays a critical role in the occurrence and progression of tumors by regulating RNA metabolism, including translocation, mRNA stability or decay, pre-mRNA splicing, and lncRNA processing. Numerous studies have shown that m6A modification is involved in the development of various cancers. This review aims to summarize the significant role of m6A modification in the proliferation and tumorigenesis of CRC, as well as the potential of modulating m6A modification for tumor treatment. These findings may offer new therapeutic strategies for clinical implementation of m6A modification in CRC in the near future.

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“…In 5‐fluorouracil (5‐FU)‐resistant CRC cells, METTL3 elevates LDHA translation, thereby enhancing glycolysis and 5‐FU chemoresistance 350 . METTL3 induces the upregulation of LINC01615, thereby increasing glucose‐6‐phosphate dehydrogenase (G6PD) expression, increasing the PPP flux, sustaining cell survival, and modulating oxaliplatin chemosensitivity under conditions of nutrient deprivation 351 . Knockout of METTL3 in xenograft mouse tumor model also exhibits the impaired glucose uptake and inhibited tumor growth.…”

Section: Rna Methylation and Cancer Metabolismmentioning

confidence: 99%

“… 350 METTL3 induces the upregulation of LINC01615, thereby increasing glucose‐6‐phosphate dehydrogenase (G6PD) expression, increasing the PPP flux, sustaining cell survival, and modulating oxaliplatin chemosensitivity under conditions of nutrient deprivation. 351 Knockout of METTL3 in xenograft mouse tumor model also exhibits the impaired glucose uptake and inhibited tumor growth. METTL3 has been observed to upregulate and maintain GLUT1 and HK2 expression.…”

Section: Rna Methylation and Cancer Metabolismmentioning

confidence: 99%

Critical roles and clinical perspectives of RNA methylation in cancer

Li,

Yao,

Liu

et al. 2024

MedComm

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RNA modification, especially RNA methylation, is a critical posttranscriptional process influencing cellular functions and disease progression, accounting for over 60% of all RNA modifications. It plays a significant role in RNA metabolism, affecting RNA processing, stability, and translation, thereby modulating gene expression and cell functions essential for proliferation, survival, and metastasis. Increasing studies have revealed the disruption in RNA metabolism mediated by RNA methylation has been implicated in various aspects of cancer progression, particularly in metabolic reprogramming and immunity. This disruption of RNA methylation has profound implications for tumor growth, metastasis, and therapy response. Herein, we elucidate the fundamental characteristics of RNA methylation and their impact on RNA metabolism and gene expression. We highlight the intricate relationship between RNA methylation, cancer metabolic reprogramming, and immunity, using the well‐characterized phenomenon of cancer metabolic reprogramming as a framework to discuss RNA methylation's specific roles and mechanisms in cancer progression. Furthermore, we explore the potential of targeting RNA methylation regulators as a novel approach for cancer therapy. By underscoring the complex mechanisms by which RNA methylation contributes to cancer progression, this review provides a foundation for developing new prognostic markers and therapeutic strategies aimed at modulating RNA methylation in cancer treatment.

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LINC01615 maintains cell survival in adaptation to nutrient starvation through the pentose phosphate pathway and modulates chemosensitivity in colorectal cancer

Cited by 15 publications

References 58 publications

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

m6A modification on the fate of colorectal cancer: functions and mechanisms of cell proliferation and tumorigenesis

Critical roles and clinical perspectives of RNA methylation in cancer

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