Significance of stratifin in early progression of lung adenocarcinoma and its potential therapeutic relevance

Shiba-Ishii, Aya

doi:10.1111/pin.13147

Cited by 16 publications

(12 citation statements)

References 67 publications

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“…In the present study, patients with lung adenocarcinoma (LUAD), the most common histological subtype of lung cancer ( Shiba-Ishii, 2021 ; Succony et al, 2021 ), were subclassified into three molecular subtypes based on the expression of m7G-associated genes. Differentially expressed genes (DEGs) among the three subtypes were screened and used to further stratify the patients into two gene-clusters.…”

Section: Introductionmentioning

confidence: 99%

m7G-Associated subtypes, tumor microenvironment, and validation of prognostic signature in lung adenocarcinoma

Wang

Zhao

et al. 2022

Front. Genet.

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Background: 7-Methylguanosine (m7G) is an important posttranscriptional modification that regulates gene expression and is involved in tumorigenesis and development. Tumor microenvironment has been proven to be highly involved in tumor progression and prognosis. However, how m7G-associated genes affect the tumor microenvironment of patients with lung adenocarcinoma (LUAD) remains to be further clarified.Methods: The genetic alterations of m7G-associated genes and their associations with the prognosis and tumor microenvironment in LUAD patients were systemically analyzed. An m7G-Riskscore was established and analyzed for its performance in disease prognosis and association with patient response to immunotherapy. Expression of the model genes at the protein level was investigated through ex vivo experiments. A nomogram was finally obtained based on the m7G-Riskscore and several significant clinical pathological features.Results: m7G-Associated genes were obtained from five LUAD datasets from The Cancer Genome Atlas and Gene Expression Omnibus databases, and their expression pattern was determined. Based on the m7G-associated genes, three LUAD clusters were defined. The differentially expressed genes from the three clusters were screened and used to further divide the LUAD patients into two gene clusters. It was demonstrated that the alterations of m7G-associated genes were associated with the clinical pathological features, prognosis, and tumor immune infiltration in LUAD patients. An m7G-Riskscore including CAND1, RRM2, and SLC2A1 was obtained with robust and accurate prognostic performance. WB and cell immunofluorescence also showed significant dysregulation of CAND1, RRM2, and SLC2A1 in LUAD. In addition, a nomogram was established to improve the clinical feasibility of the m7G-Riskscore. Correlation analysis revealed that patients with a lower m7G-Riskscore had higher immune and stromal scores, responded well to chemotherapeutics and multiple targeted drugs, and survived longer. Patients with a higher m7G-Riskscore tended to suffer from a higher tumor mutation burden. Furthermore, the m7G-Riskscore exhibited significant associations with immune cell infiltration and cancer stemness.Conclusion: This study systemically analyzed m7G-associated genes and identified their potential role in tumor microenvironment and prognosis in patients with LUAD. The findings of the present study may help better understand LUAD from the m7G perspective and also provide a new thought toward the prognosis and treatment of LUAD.

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Section: Introductionmentioning

confidence: 99%

m7G-Associated subtypes, tumor microenvironment, and validation of prognostic signature in lung adenocarcinoma

Wang

Zhao

et al. 2022

Front. Genet.

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“…SFN gene encodes a protein participating in regulating epithelial-mesenchymal interaction ( Asdaghi et al, 2012 ). Aya Shiba-Ishii reported that SFN promoted early progression of LUAD by activating cell proliferation ( Shiba‐Ishii, 2021 ). SSBP1, MRE11 and FZD7 have been considered as potential treatment sites of LUAD ( Sun et al, 2017 ; Wang et al, 2017 ; Zeng et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Characterization of lung adenocarcinoma based on immunophenotyping and constructing an immune scoring model to predict prognosis

Liu

Xiao

et al. 2022

Front. Pharmacol.

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Background: Lung cancer poses great threat to human health, and lung adenocarcinoma (LUAD) is the main subtype. Immunotherapy has become first line therapy for LUAD. However, the pathogenic mechanism of LUAD is still unclear.Methods: We scored immune-related pathways in LUAD patients using single sample gene set enrichment analysis (ssGSEA) algorithm, and further identified distinct immune-related subtypes through consistent clustering analysis. Next, immune signatures, Kaplan-Meier survival analysis, copy number variation (CNV) analysis, gene methylation analysis, mutational analysis were used to reveal differences between subtypes. pRRophetic method was used to predict the response to chemotherapeutic drugs (half maximal inhibitory concentration). Then, weighted gene co-expression network analysis (WGCNA) was performed to screen hub genes. Significantly, we built an immune score (IMscore) model to predict prognosis of LUAD.Results: Consensus clustering analysis identified three LUAD subtypes, namely immune-Enrich subtype (Immune-E), stromal-Enrich subtype (Stromal-E) and immune-Deprived subtype (Immune-D). Stromal-E subtype had a better prognosis, as shown by Kaplan-Meier survival analysis. Higher tumor purity and lower immune cell scores were found in the Immune-D subtype. CNV analysis showed that homologous recombination deficiency was lower in Stromal-E and higher in Immune-D. Likewise, mutational analysis found that the Stromal-E subtype had a lower mutation frequency in TP53 mutations. Difference in gene methylation (ZEB2, TWIST1, CDH2, CDH1 and CLDN1) among three subtypes was also observed. Moreover, Immune-E was more sensitive to traditional chemotherapy drugs Cisplatin, Sunitinib, Crizotinib, Dasatinib, Bortezomib, and Midostaurin in both the TCGA and GSE cohorts. Furthermore, a 6-gene signature was constructed to predicting prognosis, which performed better than TIDE score. The performance of IMscore model was successfully validated in three independent datasets and pan-cancer.

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“… 1 Recent studies have shown that toll‐like receptors (TLRs) are expressed in lung cancers, suggesting that TLRs may be implicated in lung cancer progression. 2 , 3 Although several studies have shown that stratifin ( SFN , 14‐3‐3 sigma) facilitated lung cancer development and progression, 4 , 5 , 6 the molecular and cellular mechanisms by which SFN is functionally involved in lung cancer progression, and the role of SFN in lung cancer progression in response to extrinsic stimulation, such as TLR agonist, are largely unknown. Here, we show that SFN expression is remarkably up‐regulated in lung cancer tissues through The Cancer Genome Atlas (TCGA) data and primary non‐small cell lung cancers ( n = 31 of our cohort patients) analysis, and SFN positively regulates lung cancer progression through the autophagy induction by facilitating TRAF6‐ Vps34‐BECN1 complex in response to an extrinsic TLR4 agonist.…”

Section: Figurementioning

confidence: 99%

“…Mi-Jeong Kim 1 Ji Su Lee 1 Juhee Son 1 Duk-Hwan Kim 2 Joo Sang Lee 3 Soo-Kyung Jeong 4 Eunyoung Chun 4 Ki-Young Lee 1,5,6,7…”

mentioning

confidence: 99%

Stratifin (SFN) regulates lung cancer progression via nucleating the Vps34‐BECN1‐TRAF6 complex for autophagy induction

Kim

Son

et al. 2022

Clinical & Translational Med

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Significance of stratifin in early progression of lung adenocarcinoma and its potential therapeutic relevance

Cited by 16 publications

References 67 publications

m7G-Associated subtypes, tumor microenvironment, and validation of prognostic signature in lung adenocarcinoma

m7G-Associated subtypes, tumor microenvironment, and validation of prognostic signature in lung adenocarcinoma

Characterization of lung adenocarcinoma based on immunophenotyping and constructing an immune scoring model to predict prognosis

Stratifin (SFN) regulates lung cancer progression via nucleating the Vps34‐BECN1‐TRAF6 complex for autophagy induction

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