Emerging role of LINC00461 in cancer

Zhang, Qiudan; Zhong, Chenming; Shen, Jinze; Sang, Chen; Jia, Yunhua; Duan, Shiwei

doi:10.1016/j.biopha.2022.113239

Cited by 13 publications

(11 citation statements)

References 56 publications

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“…In the TME, the accumulation of cytokines, chemokines, soluble factors, and a mixture of biomolecules in exosomes compromises the immune response during the advanced stages of cancer (156)(157)(158). Soluble factors with immunosuppressant activity, such as IL-10, TGF-b, IL-4, IL-6, etc., impair the function of NK cells (159, 160) and CTLs (161,162) by inhibiting their effector activity and downregulating the expression of transcripts coding for cytolytic molecules.…”

Section: Ifn-g Macrophages Nk and T-cellsmentioning

confidence: 99%

The systemic-level repercussions of cancer-associated inflammation mediators produced in the tumor microenvironment

et al. 2022

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The tumor microenvironment is a dynamic, complex, and redundant network of interactions between tumor, immune, and stromal cells. In this intricate environment, cells communicate through membrane–membrane, ligand–receptor, exosome, soluble factors, and transporter interactions that govern cell fate. These interactions activate the diverse and superfluous signaling pathways involved in tumor promotion and progression and induce subtle changes in the functional activity of infiltrating immune cells.The immune response participates as a selective pressure in tumor development. In the early stages of tumor development, the immune response exerts anti-tumor activity, whereas during the advanced stages, the tumor establishes mechanisms to evade the immune response, eliciting a chronic inflammation process that shows a pro-tumor effect.The deregulated inflammatory state, in addition to acting locally, also triggers systemic inflammation that has repercussions in various organs and tissues that are distant from the tumor site, causing the emergence of various symptoms designated as paraneoplastic syndromes, which compromise the response to treatment, quality of life, and survival of cancer patients. Considering the tumor–host relationship as an integral and dynamic biological system, the chronic inflammation generated by the tumor is a communication mechanism among tissues and organs that is primarily orchestrated through different signals, such as cytokines, chemokines, growth factors, and exosomes, to provide the tumor with energetic components that allow it to continue proliferating. In this review, we aim to provide a succinct overview of the involvement of cancer-related inflammation at the local and systemic level throughout tumor development and the emergence of some paraneoplastic syndromes and their main clinical manifestations. In addition, the involvement of these signals throughout tumor development will be discussed based on the physiological/biological activities of innate and adaptive immune cells. These cellular interactions require a metabolic reprogramming program for the full activation of the various cells; thus, these requirements and the by-products released into the microenvironment will be considered. In addition, the systemic impact of cancer-related proinflammatory cytokines on the liver—as a critical organ that produces the leading inflammatory markers described to date—will be summarized. Finally, the contribution of cancer-related inflammation to the development of two paraneoplastic syndromes, myelopoiesis and cachexia, will be discussed.

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Section: Ifn-g Macrophages Nk and T-cellsmentioning

confidence: 99%

The systemic-level repercussions of cancer-associated inflammation mediators produced in the tumor microenvironment

et al. 2022

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“…According to NONCODEV5 dataset in the human genome over 100,000 lncRNA exist 5 . Numerous studies have shown that lncRNAs regulate many cellular processes, including proliferation, differentiation, cell cycle, apoptosis, drug resistance, epigenetic modifications, RNA/protein stability, transcription, translation and post‐transcriptional modifications 6–8 . LncRNA Survival Associated Mitochondrial Melanoma Specific Oncogenic Non‐coding RNA (SAMMSON), also known as LINC01212, has been identified by Leucci and colleagues 9 .…”

Section: Introductionmentioning

confidence: 99%

“… 5 Numerous studies have shown that lncRNAs regulate many cellular processes, including proliferation, differentiation, cell cycle, apoptosis, drug resistance, epigenetic modifications, RNA/protein stability, transcription, translation and post‐transcriptional modifications. 6 , 7 , 8 LncRNA Survival Associated Mitochondrial Melanoma Specific Oncogenic Non‐coding RNA (SAMMSON), also known as LINC01212, has been identified by Leucci and colleagues. 9 SAMMSON is located on the 3p13 chromosome and exists 4 exons and 28 transcripts that are produced through alternative splicing ( https://asia.ensembl.org/Homo_sapiens/Gene/Splice?db=core;g=ENSG00000240405;r=3:69999550‐70518064 ).…”

Section: Introductionmentioning

confidence: 99%

The oncogenic role of SAMMSON lncRNA in tumorigenesis: A comprehensive review with especial focus on melanoma

Ghasemian,

Babaahmadi‐Rezaei,

Khedri

et al. 2023

J Cellular Molecular Medi

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LncRNA Survival Associated Mitochondrial Melanoma Specific Oncogenic Non‐coding RNA (SAMMSON) is located on human chromosome 3p13, and its expression is upregulated in several tumours, including melanoma, breast cancer, glioblastoma and liver cancer and has an oncogenic role in malignancy disorders. It has been reported that SAMMSON impacts metabolic regulation, cell proliferation, apoptosis, EMT, drug resistance, invasion and migration. Also, SAMMSON is involved in regulating several pathways such as Wnt, MAPK, PI3K, Akt, ERK and p53. SAMMSON is considered a potential diagnostic and prognostic biomarker in several types of cancer and a suitable therapeutic target. In addition, the highly expressed SAMMSON is closely associated with clinicopathological features of various cancers. SAMMSON has a significant role in regulating epigenetic processes by regulating histone protein or the status of DNA methylation. Herein for the first time, we comprehensively summarized the currently available SAMMSON, molecular regulatory pathways, and clinical significance. We believe that clarifying all the molecular aspects of this lncRNA can be a good guide for cancer studies in the future.

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“…Next-generation sequencing technology has shown that most of the human genome can be transcribed into non-coding RNA (ncRNA), including microRNA (miRNA), circular RNA (circRNA), long non-coding RNA (lncRNA), and pseudogenes ( 1 ). ncRNAs play regulatory roles at gene transcription and post-transcription levels, and their abnormal expression is often associated with the pathogenesis of various diseases ( 2 , 3 ). Among them, lncRNAs have been shown to regulate various gene expression processes.…”

Section: Introductionmentioning

confidence: 99%

LINC00324 in cancer: Regulatory and therapeutic implications

et al. 2022

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LINC00324 is a 2082 bp intergenic noncoding RNA. Aberrant expression of LINC00324 was associated with the risk of 11 tumors and was closely associated with clinicopathological features and prognostic levels of 7 tumors. LINC00324 can sponge multiple miRNAs to form complex ceRNA networks, and can also recruit transcription factors and bind RNA-binding protein HuR, thereby regulating the expression of a number of downstream protein-coding genes. LINC00324 is involved in 4 signaling pathways, including the PI3K/AKT signaling pathway, cell cycle regulatory pathway, Notch signaling pathway, and Jak/STAT3 signaling pathway. High expression of LINC00324 was associated with larger tumors, a higher degree of metastasis, a higher TNM stage and clinical stage, and shorter OS. Currently, four downstream genes in the LINC00324 network have targeted drugs. In this review, we summarize the molecular mechanisms and clinical value of LINC00324 in tumors and discuss future directions and challenges for LINC00324 research.

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Emerging role of LINC00461 in cancer

Cited by 13 publications

References 56 publications

The systemic-level repercussions of cancer-associated inflammation mediators produced in the tumor microenvironment

The systemic-level repercussions of cancer-associated inflammation mediators produced in the tumor microenvironment

The oncogenic role of SAMMSON lncRNA in tumorigenesis: A comprehensive review with especial focus on melanoma

LINC00324 in cancer: Regulatory and therapeutic implications

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