Bioinformatics analysis of differentially expressed genes in tumor and paracancerous tissues of patients with lung adenocarcinoma

Yang, Rong; Zhou, Yuwei; Du, Chengli; Wu, Yihe

doi:10.21037/jtd-20-3453

Cited by 9 publications

(5 citation statements)

References 17 publications

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“…Our study provides novel insights into the role of Claudin5 in ESCC. We found that Claudin5 expression is suppressed in ESCC tumors, consistent with previous findings in other cancer types such as lung cancer [ 21 , 22 ], breast cancer [ 23 ], and colon cancer [ 24 ]. Moreover, our functional experiments revealed the specific effects of Claudin5 on cells proliferation, migration, invasion, and radiosensitivity in ESCC.…”

Section: Discussionsupporting

confidence: 91%

Downregulation of Claudin5 promotes malignant progression and radioresistance through Beclin1-mediated autophagy in esophageal squamous cell carcinoma

Huang¹,

Zhang²,

Li³

et al. 2023

J Transl Med

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Background Esophageal squamous cell carcinoma (ESCC) is a highly prevalent and aggressive cancer with poor treatment outcomes. Despite the critical role of tight junction proteins in tumorigenesis, the involvement of Claudin5 in ESCC remains poorly understood. Thus, this study aimed to investigate the role of Claudin5 in ESCC malignant progression and radioresistance, as well as the underlying regulatory mechanisms. Methods The expression of Claudin5 was evaluated in esophageal cancer tissue using both public databases and 123 clinical samples. CCK-8, transwell invasion, wound healing and clonogenic survival assays were used to examine the proliferation, invasion, migration and radiosensitivity of ESCC cells in vitro. Xenograft and animal lung metastasis experiments were conducted to examine the impact of Claudin5 on tumor growth and lung metastasis in vivo. The effect of Claudin5 on autophagy was detected via transmission electron microscopy, western blotting and autophagy flux. Immunohistochemical staining was used to detect Claudin5 expression in ESCC patient samples. The statistical difference was assessed with Student t test or one-way ANOVA. The correlation between Claudin5 expression and radiotherapy response rate was performed by the Chi-square test. The significance of Kaplan–Meier curves was evaluated by the Logrank test. Results Claudin5 expression was downregulated in ESCC tissues. Downregulation of Claudin5 promoted ESCC cell proliferation, invasion, and migration both in vitro and in vivo. Downregulation of Claudin5 decreased the radiosensitivity of ESCC cells. Moreover, downregulation of Claudin5 promoted autophagy and the expression of Beclin1. Beclin1 knockdown reversed the effect of Claudin5 downregulation on autophagy induction and the promotion of ESCC cell malignant progression and radioresistance. Additionally, low expression of Claudin5 in ESCC cancer tissues was associated with poor radiotherapy response and prognosis. Conclusions In summary, these findings suggest that downregulation of Claudin5 promotes ESCC malignant progression and radioresistance via Beclin1-autophagy activation and may serve as a promising biomarker for predicting radiotherapy response and patient outcome in ESCC.

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Section: Discussionsupporting

confidence: 91%

Downregulation of Claudin5 promotes malignant progression and radioresistance through Beclin1-mediated autophagy in esophageal squamous cell carcinoma

Huang¹,

Zhang²,

Li³

et al. 2023

J Transl Med

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“…However, to date, there is a lack of systematic studies on miR-126-5p and miR-218-5p expression levels in LUAD and their mechanisms of action. Collagen type I alpha 1 chain (COL1A1) is confirmed to be an extracellular matrix protein that is overexpressed in many types of malignant tumors, including lung, breast, and colorectal tumors [ 18 – 20 ]. In addition, differential expression of COL1A1 predicts poor clinical outcomes (e.g., lymph node metastasis) in lung squamous cell carcinoma patients [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00511 promotes COL1A1-mediated proliferation and metastasis by sponging miR-126-5p/miR-218-5p in lung adenocarcinoma

et al. 2022

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Background Lung adenocarcinoma (LUAD) is currently the leading cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) play key roles in tumor occurrence and development as crucial cancer regulators. The present study aimed to explore the molecular mechanism and regulatory network of Linc00511 in LUAD and to identify new potential therapeutic targets for LUAD. Methods Real-time quantitative polymerase chain reaction (RT–qPCR) was performed to determine the relative Linc00511 levels in LUAD tissues and cells. The proliferation, apoptosis, migration, and invasion abilities of LUAD cells were assessed by a Cell Counting Kit-8 (CCK-8) assay, a colony formation assay, flow cytometry, and a Transwell assay. Changes in hsa_miR-126-5p, hsa_miR-218-5p, and COL1A1 expression were analyzed using western blotting and RT–qPCR. Targeted binding between miR-126-5p/miR-218-5p and Linc00511 or COL1A1 was verified with a luciferase reporter system and confirmed by an RNA pulldown assay. The participation of the PI3K/AKT signaling pathway was confirmed via western blotting. Xenograft animal experiments were performed to detect the impact of Linc00511 on LUAD tumor growth in vivo. Results In the present work, we observed that Linc00511 was upregulated in LUAD tissues and cells. Loss/gain-of-function experiments indicated that knockdown of Linc00511 significantly inhibited LUAD cell proliferation, migration and invasion and promoted LUAD cell apoptosis, whereas overexpression of Linc00511 showed the opposite effects. In addition, we determined that Linc00511 promoted COL1A1-mediated cell proliferation and cell motility by sponging miR-126-5p and miR-218-5p. Moreover, Linc00511 activated the PI3K/AKT signaling pathway through upregulation of COL1A1. Finally, silencing of Linc00511 inhibited LUAD tumor growth in vivo. Conclusions Linc00511 acts as a competing endogenous RNA to regulate COL1A1 by targeting miR-126-5p and miR-218-5p, thereby promoting the proliferation and invasion of LUAD cells.

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“…It is mainly used to process and analyze biological data via mathematical formulas and statistical methods[ 24 ]. Numerous studies have investigated biomarkers related to LUAD[ 25 , 26 ], but research conducted thus far has not identified effective biomarkers. It is therefore crucial to analyze LUAD from various aspects, identify the best target molecules for its treatment, and elucidate the biological pathways underlying its development and progression.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and biological pathways in lung adenocarcinoma by integrated bioinformatics analysis

Zhang¹,

Liu²,

Zhuang³

et al. 2023

World J Clin Cases

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Hepatocellular carcinoma (HCC) is one of the most prevalent tumors worldwide and the leading contributor to cancer-related deaths. The progression and metastasis of HCC are closely associated with altered mitochondrial metabolism, including mitochondrial stress response. Mitokines, soluble proteins produced and secreted in response to mitochondrial stress, play an essential immunomodulatory role. Immunotherapy has emerged as a crucial treatment option for HCC. However, a positive response to therapy is typically dependent on the interaction of tumor cells with immune regulation within the tumor microenvironment. Therefore, exploring the specific immunomodulatory mechanisms of mitokines in HCC is essential for improving the efficacy of immunotherapy. This study provides a comprehensive overview of the association between HCC and the immune microenvironment and highlights recent progress in understanding the involvement of mitochondrial function in preserving liver function. In addition, a systematic review of mitokines-mediated immunomodulation in HCC is presented. Finally, the potential diagnostic and therapeutic roles of mitokines in HCC are prospected and summarized. Recent progress in mitokine research represents a new prospect for mitochondrial therapy. Considering the potential of mitokines to regulate immune function, investigating them as a relevant molecular target holds great promise for the diagnosis and treatment of HCC.

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Bioinformatics analysis of differentially expressed genes in tumor and paracancerous tissues of patients with lung adenocarcinoma

Cited by 9 publications

References 17 publications

Downregulation of Claudin5 promotes malignant progression and radioresistance through Beclin1-mediated autophagy in esophageal squamous cell carcinoma

Downregulation of Claudin5 promotes malignant progression and radioresistance through Beclin1-mediated autophagy in esophageal squamous cell carcinoma

LncRNA LINC00511 promotes COL1A1-mediated proliferation and metastasis by sponging miR-126-5p/miR-218-5p in lung adenocarcinoma

Identification of key genes and biological pathways in lung adenocarcinoma by integrated bioinformatics analysis

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