Long noncoding <scp>RNA LINC01419</scp> promotes hepatocellular carcinoma malignancy by mediating <scp>miR</scp>‐485‐5p/<scp>LSM4</scp> axis

Sun, Zengpeng; Tan, Zhiguo; Peng, Chuang

doi:10.1002/kjm2.12566

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…High LSM4 expression enhanced ovarian cancer cell proliferation, metastasis and glycolysis 28 . LSM4 had increased expression in hepatocellular carcinoma and could serve as a diagnostic marker, which upregulation contributed to cell malignant behaviors 29,30 . Although LSM4 has been shown to be oncogenic in many cancers, its role in NSCLC progression has not been explored.…”

Section: Discussionmentioning

confidence: 99%

“… 28 LSM4 had increased expression in hepatocellular carcinoma and could serve as a diagnostic marker, which upregulation contributed to cell malignant behaviors. 29 , 30 Although LSM4 has been shown to be oncogenic in many cancers, its role in NSCLC progression has not been explored. Database analysis revealed that LSM4 expression was high in LUAD tissues and could be decreased by SF3B4 knockdown in NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

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METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression

He,

Gu,

Wei

et al. 2024

Thoracic Cancer

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BackgroundSplicing factor B subunit 4 (SF3B4) has been confirmed to participate in the progression of many cancers and is considered to be a potential target for non‐small cell lung cancer (NSCLC). Thus, the role and molecular mechanism of SF3B4 in NSCLC progression deserves further study.MethodsQuantitative real‐time PCR and western blot were employed to detect the mRNA and protein levels of SF3B4, Sm‐like protein 4 (LSM4) and methyltransferase‐like 3 (METTL3). Cell proliferation, apoptosis, invasion, migration and stemness were tested by cell counting kit‐8, colony formation, flow cytometry, transwell, wound healing, and sphere formation assays. The interaction between SF3B4 and METTL3 or LSM4 was confirmed by MeRIP, RIP and Co‐IP assays. Mice xenograft models were constructed to assess the effects of METTL3 and SF3B4 on NSCLC tumorigenesis.ResultsSF3B4 had high expression in NSCLC tissues and was associated with the shorter overall survival of NSCLC patients. Knockdown of SF3B4 suppressed NSCLC cell proliferation, invasion, migration and stemness, while inducing apoptosis. METTL3 promoted SF3B4 mRNA stability by m6A modification, and its knockdown inhibited NSCLC cell growth, metastasis and stemness by downregulating SF3B4. SF3B4 could interact with LSM4, and sh‐SF3B4‐mediated the inhibition on NSCLC cell functions could be reversed by LSM4 overexpression. In addition, reduced METTL3 expression restrained NSCLC tumor growth, and this effect was reversed by SF3B4 overexpression.ConclusionMETTL3‐stablized SF3B4 promoted NSCLC cell growth, metastasis and stemness via positively regulating LSM4.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression

He,

Gu,

Wei

et al. 2024

Thoracic Cancer

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“…LSM4 has also been found to be upregulated in several types of cancer, such as breast cancer, and in early-stage pancreatic ductal adenocarcinoma, where it is associated with a poor prognosis [ 3 , 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Yeast Lsm Pro-Apoptotic Mutants Show Defects in Autophagy

Caraba,

Stirpe,

Palermo

et al. 2023

IJMS

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LSM4 is an essential yeast gene encoding a component of different LSM complexes involved in the regulation of mRNA splicing, stability, and translation. In previous papers, we reported that the expression in S. cerevisiae of the K. lactis LSM4 gene lacking the C-terminal Q/N-rich domain in an Lsm4 null strain S. cerevisiae (Sclsm4Δ1) restored cell viability. Nevertheless, in this transformed strain, we observed some phenotypes that are typical markers of regulated cell death, reactive oxygen species (ROS), and oxidated RNA accumulation. In this paper, we report that a similar truncation operated in the S. cerevisiae LSM4 gene confers on cells the same phenotypes observed with the K. lactis lsm4Δ1 gene. Up until now, there was no evidence of the direct involvement of LSM4 in autophagy. Here we found that the Sclsm4Δ1 mutant showed a block in the autophagic process and was very sensitive to nitrogen starvation or treatment with low doses of rapamycin, an inducer of autophagy. Moreover, both during nitrogen starvation and aging, the Sclsm4Δ1 mutant accumulated cytoplasmic autophagy-related structures, suggesting a role of Lsm4 in a later step of the autophagy process.

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Role of Non-Coding RNAs in Hepatocellular Carcinoma Progression: From Classic to Novel Clinicopathogenetic Implications

Romeo,

Dallio,

Scognamiglio

et al. 2023

Cancers

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Hepatocellular carcinoma (HCC) is a predominant malignancy with increasing incidences and mortalities worldwide. In Western countries, the progressive affirmation of Non-alcoholic Fatty Liver Disease (NAFLD) as the main chronic liver disorder in which HCC occurrence is appreciable even in non-cirrhotic stages, constitutes a real health emergency. In light of this, a further comprehension of molecular pathways supporting HCC onset and progression represents a current research challenge to achieve more tailored prognostic models and appropriate therapeutic approaches. RNA non-coding transcripts (ncRNAs) are involved in the regulation of several cancer-related processes, including HCC. When dysregulated, these molecules, conventionally classified as “small ncRNAs” (sncRNAs) and “long ncRNAs” (lncRNAs) have been reported to markedly influence HCC-related progression mechanisms. In this review, we describe the main dysregulated ncRNAs and the relative molecular pathways involved in HCC progression, analyzing their implications in certain etiologically related contexts, and their applicability in clinical practice as novel diagnostic, prognostic, and therapeutic tools. Finally, given the growing evidence supporting the immune system response, the oxidative stress-regulated mechanisms, and the gut microbiota composition as relevant emerging elements mutually influencing liver-cancerogenesis processes, we investigate the relationship of ncRNAs with this triad, shedding light on novel pathogenetic frontiers of HCC progression.

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Long noncoding RNA LINC01419 promotes hepatocellular carcinoma malignancy by mediating miR‐485‐5p/LSM4 axis

Cited by 4 publications

References 31 publications

METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression

METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression

Yeast Lsm Pro-Apoptotic Mutants Show Defects in Autophagy

Role of Non-Coding RNAs in Hepatocellular Carcinoma Progression: From Classic to Novel Clinicopathogenetic Implications

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