The construction and analysis of tumor-infiltrating immune cells and ceRNA networks in metastatic adrenal cortical carcinoma

Huang, Runzhi; Liu, Ziqi; Tian, Tingli; Song, Dianwen; Yan, Penghui; Yin, Huabin; Hu, Peng; Zhu, Xiaolong; Liu, Yihan; Li, Zhenyu; Meng, Tong; Zhang, Jie; Huang, Zongqiang

doi:10.1042/bsr20200049

Cited by 13 publications

(17 citation statements)

References 44 publications

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“…Many studies also have shown that CD8+ T cells usually mean a better prognosis among cancer patients [44,45]. M0 macrophages were reported to be inversely associated with patients' outcomes in various, such as adrenal cortical carcinoma and lung cancer [46,47]. Nowadays, majority studies evaluated the degree of smoking based on the frequency of tobacco use to define heavy smokers and light smokers without uniform quantifying standards [48][49][50].…”

Section: Discussionmentioning

confidence: 99%

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

2020

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Few studies have examined the association between smoking status (including former smokers) at diagnosis and overall survival among cancer patients. We aimed to assess the benefits of quitting smoking on cancer prognosis in cohorts of cancer patient smokers obtained from the Cancer Genome Atlas (TCGA) database. Hazard ratios (HR) were calculated to evaluate smoking behavior at cancer diagnosis (reformed smokers vs. current smokers) in association with overall survival using multivariate‐adjusted Cox regressions analysis. According to our analyses, quitting smoking was the independent protective factor for overall survival in lung squamous cell carcinoma (LUSC) (HR = 0.67, 95% CI = 0.48–0.94). Comprehensive analysis of multicomponent data across reformed and current smokers identified a total of 85 differential expressed genes (DEGs) affected by different modes of genetic and epigenetic regulation, potentially representing cancer drivers in smokers. Moreover, we provided a smoking‐associated gene expression signature, which could evaluate the true effect on prognosis with high power (HR = 1.70, 95% CI = 1.19–2.43, AUC = 0.65, 0.67, and 0.70 for 2‐, 3‐, and 5‐year survival, respectively). This signature was also applicable in other smoking‐related cancers, including bladder urothelial carcinoma (HR = 1.70, 95% CI = 1.01–2.88), cervical carcinoma (HR = 5.69, 95% CI = 1.37–23.69), head and neck squamous cell carcinoma (HR = 1.97, 95% CI = 1.41–2.76), lung adenocarcinoma (HR = 1.73, 95% CI = 1.16–2.57), and pancreatic adenocarcinoma (HR = 4.28, 95% CI = 1.47–12.47). In conclusion, this study demonstrates that quitting smoking at diagnosis decreases risk of death in cancer patients. We also provide a smoking‐associated gene expression signature to evaluate the effect of smoking on survival. Lastly, we suggest that smoking cessation could comprise a part of cancer treatment to improve survival rates of cancer patients.

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Section: Discussionmentioning

confidence: 99%

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

2020

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“…However, the intrinsic heterogeneity of tumor often engenders homogeneous cancer subtypes possessing distinct molecular features and therapeutic responses, which could invalidate most of the biomarkers from previous studies. Emerging studies have incorporated tumor heterogeneity in ceRNA network analyses 46,47 but works considering key driver mutations were scarce. Interestingly, the DEGs identi ed in patients separated by TP53 mutational status were enriched in similar pathways, denoting that the effect conferred by TP53 anomaly should be investigated in a more microcosmic way, e.g.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of a ceRNA network associated with TP53 mutations in liver hepatocellular carcinoma

Yuan¹,

Xu²,

Gan³

et al. 2022

Preprint

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Liver cancer is one of the most common causes of cancer-related death and is quantitatively dominated by the liver hepatocellular carcinoma (HCC) subtype. Although advances have been made in recent years, further exploration on new HCC carcinogenic mechanisms as well as diagnostic and therapeutic methods in the context of detrimental TP53 abnormalities is indispensable on the way to conquer HCC. In this study, competing endogenous RNA (ceRNA) network was constructed on tumor samples stratified by the TP53 mutational status. With demonstrated TP53 mutant-specificity, the network nodes including AC017104.6, RP5-1092A11.5, RP11-365O16.6 and PTBP1 were all prognosis-related. Further therapeutic correlation analysis unveiled the connection between their expressions and tumor microenvironment fluctuation as well as possible chemotherapy resistance. Additionally, we explored the drug sensitivity difference between TP53 wild type and mutant samples, complementing the therapeutic arsenal of HCC. The universality of the key node PTBP1 was verified by multi-source transcriptional and protein level expressions. Taken together, this is the first study focusing on the ceRNA network mediated by TP53 mutations and its provoked therapeutic associations in HCC. Our results deepened the understanding of the concomitant alternations brought by TP53 mutations and could benefit future therapeutic development in HCC.

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“…M0 macrophages can polarize into M1 and M2 macrophages in different environments, and evidence accumulated from many cancer models demonstrated that M1 macrophages possess inflammation-promoting characteristics, which activate cytotoxic anti-tumor mechanisms ( 25 ). According to Huang et al., the degree of M0 macrophage infiltration was significantly higher in metastatic ACC than in non-metastatic patients ( 26 ). Notably, the immune risk may lead to the suppression of M1 macrophage infiltration and the promotion of M0 infiltration, which suggests that high immune risk may contribute to tumor immune escape and poor prognosis in patients with ACC.…”

Section: Discussionmentioning

confidence: 99%

Oncogene or tumor suppressor gene: An integrated pan-cancer analysis of NBPF1

Chen

Tang

et al. 2022

Front. Endocrinol.

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Neuroblastoma breakpoint family, member 1 (NBPF1), appears to be a double-edged sword with regard to its role in carcinogenesis. On the one hand, the tumor-suppressing functions of NBPF1 have been definitively observed in neuroblastoma, prostate cancer, cutaneous squamous cell carcinoma, and cervical cancer. On the other hand, there is evidence that NBPF1 regulates the colony formation, invasion, and maintenance of liver cancer cells and hence functions as an oncogene. The roles of NBPF1 are strictly dependent on the biological context and type of organization. However, a systematic pan-cancer analysis has thus far not been undertaken, and the significance of NBPF1 in the occurrence and progression of many malignancies is uncertain. In this paper, bioinformatics techniques were employed to analyze NBPF1 expression across different cancers and investigate the relationship between NBPF1 and clinical features, prognosis, genetic alteration, and tumor immune microenvironment, respectively. Our results show that NBPF1 is variably expressed in distinct tumor tissues and is also closely linked to clinical outcomes. In particular, compared to other tumor types, there was a strong negative correlation between NBPF1 expression and various components of the tumor microenvironment in adrenocortical carcinoma (ACC). We thus developed an NBPF1-derived immune risk model based on NBPF1-related immune genes; ACC patients with a high-risk score tended to have a poorer prognosis, accompanied by immune hyporesponsiveness. NBPF1 can be used as a prognostic biomarker for multiple cancers. Moreover, anti-NBPF1 immunotherapy may be suitable for treating ACC patients.

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The construction and analysis of tumor-infiltrating immune cells and ceRNA networks in metastatic adrenal cortical carcinoma

Cited by 13 publications

References 44 publications

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

Comprehensive analysis of a ceRNA network associated with TP53 mutations in liver hepatocellular carcinoma

Oncogene or tumor suppressor gene: An integrated pan-cancer analysis of NBPF1

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