Neutrophils Promote Larynx Squamous Cell Carcinoma Progression via Activating the IL-17/JAK/STAT3 Pathway

Liu, Tianyi; Zong, Shimin; Jiang, Yang; Zhao, Rui; Wang, Jie; Hua, Qingquan

doi:10.1155/2021/8078646

Cited by 5 publications

(3 citation statements)

References 45 publications

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“…STAT3 has been found to undergo phosphorylation by several pro-inflammatory cytokines, including IL-17 [51]. Accumulating evidence indicates that activation of the IL-17/JAK/STAT3 pathway plays a significant role in tumor metastasis and growth [52]. Numerous studies have demonstrated that suppression of the JAK/STAT3 pathway by inhibitors can inhibit cancer cell invasion and promote apoptosis [44,53].…”

Section: Discussionmentioning

confidence: 99%

Notopterol Suppresses IL-17-Induced Proliferation and Invasion of A549 Lung Adenocarcinoma Cells via Modulation of STAT3, NF-κB, and AP-1 Activation

Inthanon,

Dejkriengkraikul,

Yodkeeree

2023

IJMS

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Interleukine-17 is a proinflammatory cytokine that promotes lung cancer growth and progression though the activation of the STAT3, NF-κB, and AP-1 signaling pathways. Therefore, blocking the IL-17-induced oncogenic pathway is a new strategy for the treatment of lung cancer. Notopterol, a furanocoumarin, has demonstrated anti-tumor effects in several types of tumors. However, its molecular function in relation to the IL-17-induced proliferation and invasion of A549 lung adenocarcinoma cells remains unknown. Here, notopterol exhibited an inhibitory effect on IL-17-promoted A549 cell proliferation and induced G0/G1 cell cycle arrest. Western blot analysis revealed that notopterol inhibited the expression of cell-cycle-regulatory proteins, including cyclin D1, cyclin E, CDK4, and E2F. Moreover, notopterol blocked IL-17-induced A549 cell migration and invasion by regulating the epithelial–mesenchymal transition (EMT) and reducing the expression of extracellular degradation enzymes. At the molecular level, notopterol treatment significantly down-regulated the IL-17-activated phosphorylation of Akt, JNK, ERK1/2, and STAT3, leading to a reduced level of transcriptional activity of NF-κB and AP-1. Collectively, our results suggest that notopterol blocks IL-17-induced A549 cell proliferation and invasion through the suppression of the MAPK, Akt, STAT3, AP-1, and NF-κB signaling pathways, as well as modulating EMT.

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Section: Discussionmentioning

confidence: 99%

Notopterol Suppresses IL-17-Induced Proliferation and Invasion of A549 Lung Adenocarcinoma Cells via Modulation of STAT3, NF-κB, and AP-1 Activation

Inthanon,

Dejkriengkraikul,

Yodkeeree

2023

IJMS

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“…Keratinization is also associated with tumor metastasis, with transformed keratinocytes invading the dermis through the BM leading to aggressive cutaneous squamous cell carcinomas with substantial metastatic potential ( 41 ). IL-17 signaling pathway is also a classic cancer-related signaling pathway, which has been extensively studied in breast cancer, colorectal cancer, and squamous cell carcinoma ( 42 – 44 ).…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance and identification of basement membrane-associated lncRNA in bladder cancer

et al. 2022

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Based on the importance of basement membrane (BM) in cancer invasion and metastasis, we constructed a BM-associated lncRNA risk model to group bladder cancer (BCa) patients. Transcriptional and clinical data of BCa patients were downloaded from The Cancer Genome Atlas (TCGA), and the expressed genes of BM-related proteins were obtained from the BM-BASE database. We download the GSE133624 chip data from the GEO database as an external validation dataset. We screened for statistically different BM genes between tumors and adjacent normal tissues. Co-expression analysis of lncRNAs and differentially expressed BM genes was performed to identify BM-related lncRNAs. Then, differentially expressed BM-related lncRNAs (DEBMlncRNAs) between tumor and normal tissues were identified. Univariate/multivariate Cox regression analysis was performed to select lncRNAs for risk assessment. LASSO analysis was performed to build a prognostic model. We constructed a model containing 8 DEBMlncRNAs (AC004034.1, AL662797.1, NR2F1-AS1, SETBP1-DT, AC011503.2, AC093010.2, LINC00649 and LINC02321). The prognostic risk model accurately predicted the prognosis of BCa patients and revealed that tumor aggressiveness and distant metastasis were associated with higher risk scores. In this model, we constructed a nomogram to assist clinical decision-making based on clinicopathological characteristics such as age, T, and N. The model also showed good predictive power for the tumor microenvironment and mutational burden. We validated the expression of eight lncRNAs using the dataset GSE133624 and two human bladder cancer cell lines (5637, BIU-87) and examined the expression and cellular localization of LINC00649 and AC011503.2 using a human bladder cancer tissue chip. We found that knockdown of LINC00649 expression in 5637 cells promoted the proliferation of 5637 cells.Our eight DEBMlncRNA risk models provide new insights into predicting prognosis, tumor invasion, and metastasis in BCa patients.

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“… 56 Numerous studies have reported that IL-17 levels are elevated in HNSCC and that targeting IL-17 production can impede tumor cell proliferation. 57 , 58 IL-17 promotes tumor cell proliferation by activating the JAK/STAT3 pathway 59 and inhibits apoptosis by blocking FAS-associated death domain protein through the PI3K/AKT pathway. Consistent with this, silencing IL-17 expression in laryngeal cancer cells triggered apoptosis through the PI3K/AKT/FAS/FASL pathway.…”

Section: Role Of Inflammation-related Mediators In the Progression Of...mentioning

confidence: 99%

The Role of Inflammation-Associated Factors in Head and Neck Squamous Cell Carcinoma

Li,

Zeng,

Liu

et al. 2023

JIR

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Head and neck squamous cell carcinoma (HNSCC), which originates in the head or neck tissues, is characterized by high rates of recurrence and metastasis. Inflammation is important in HNSCC prognosis. Inflammatory cells and their secreted factors contribute to the various stages of HNSCC development through multiple mechanisms. In this review, the mechanisms through which inflammatory factors, signaling pathways, and cells contribute to the initiation and progression of HNSCC have been discussed in detail. Furthermore, the diagnostic and therapeutic potential of targeting inflammation in HNSCC has been discussed to gain new insights into improving patient prognosis.

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Neutrophils Promote Larynx Squamous Cell Carcinoma Progression via Activating the IL-17/JAK/STAT3 Pathway

Cited by 5 publications

References 45 publications

Notopterol Suppresses IL-17-Induced Proliferation and Invasion of A549 Lung Adenocarcinoma Cells via Modulation of STAT3, NF-κB, and AP-1 Activation

Notopterol Suppresses IL-17-Induced Proliferation and Invasion of A549 Lung Adenocarcinoma Cells via Modulation of STAT3, NF-κB, and AP-1 Activation

Prognostic significance and identification of basement membrane-associated lncRNA in bladder cancer

The Role of Inflammation-Associated Factors in Head and Neck Squamous Cell Carcinoma

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