Exosomal epidermal growth factor receptor is involved in HPV-16 E7-induced epithelial-mesenchymal transition of non-small cell lung cancer cells: A driver of signaling in vivo

Zhou, Zhiyuan; Wu, Xiaofeng; Zhan, Riming; Li, Xiangyong; Cheng, D; Chen, Li; Wang, Tianyu; Yu, Hua; Zhang, Guihong; Tang, Xudong

doi:10.1080/15384047.2022.2133332

Cited by 6 publications

(3 citation statements)

References 57 publications

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“…It has been reported that HPV-infected lung cancer cells exhibited increased proliferative and invasive ability both in vitro and in vivo. Further investigation revealed that Toll-like receptor 3 (TLR3) and epidermal growth factor receptor (EGFR) were the key factors regulating the invasion and EMT capacity of lung cancer, as the inhibition of TLR3 or EGFR expression in cancer cells would significantly attenuate HPV-mediated lung cancer development [ 45 , 46 ]. Moreover, HPV can decrease the expression of p53 in lung tumors and suppress tumor cell apoptosis via upregulation of the inhibitors of apoptosis proteins (IAPs) but downregulation of Bcl-2 homologous antagonist/killer (Bak) [ 47 ].…”

Section: Virus and Lung Cancermentioning

confidence: 99%

Dark under the Lamp: Neglected Biological Pollutants in the Environment Are Closely Linked to Lung Cancer

Wang,

Chan,

Zhang

et al. 2024

IJMS

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Environmental pollutants are closely linked to lung cancer. The different types of environmental pollutants can be classified as chemical, physical, and biological. The roles of common chemical and physical pollutants such as PM2.5, smoking, radon, asbestos, and formaldehyde in lung cancer have been extensively studied. Notably, the worldwide COVID-19 pandemic raised awareness of the strong link between biological pollution and human health. Allergens such as house dust mites and pollen, as well as bacteria and viruses, are common biological pollutants. A few biological pollutants have been reported to promote lung cancer via inducing inflammatory cytokines secretion, such as IL-1β, IL-6, and TGF-β, as well as suppressing immunosurveillance by upregulating regulatory T (Treg) cells while dampening the function of CD8+ T cells and dendritic cells. However, the correlation between common biological hazards, such as SARS-CoV-2, human immunodeficiency viruses, Helicobacter pylori, and house dust mites, and lung cancer is not fully elucidated, and the underlying mechanisms are still unclear. Moreover, the majority of studies that have been performed in lung cancer and biological carcinogens were not based on the perspective of biological pollutants, which has challenged the systematicity and coherence in the field of biological pollutants in lung cancer. Here, in addition to reviewing the recent progress made in investigating the roles of allergens, viruses, and bacteria in lung cancer, we summarized the potential mechanisms underlying biological pollutants in lung cancer. Our narrative review can shed light on understanding the significance of biological pollutants in lung cancer, as well as inspire and broaden research ideas on lung cancer etiology.

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Section: Virus and Lung Cancermentioning

confidence: 99%

Dark under the Lamp: Neglected Biological Pollutants in the Environment Are Closely Linked to Lung Cancer

Wang,

Chan,

Zhang

et al. 2024

IJMS

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“… 11 Human papillomavirus can enhance the expression of EGFR in exosomes, which is involved in the epithelial-mesenchymal transition (EMT) of lung cancer cells. 12 In lung cancer, EGFR-containing exosomes can also regulate the function of T cells. 13 Moreover, EGFR in breast cancer cell-derived exosomes can activate the mitogen-activated protein kinase (MAPK) survival pathway and stimulate monocyte survival.…”

Section: Introductionmentioning

confidence: 99%

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Chen,

Ding,

et al. 2024

OTT

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Purpose Chronic gastroesophageal reflux disease (GERD) causes the abnormal reflux of acid and bile salts, which would induce Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). EGFR, as one of main components of the exosome, plays an important role in cancer progression. Here, we investigated the role of acidic bile salts (ABS)-induced exosomal EGFR in EAC cell proliferation. Methods Electronic microscopic examination and Western blot were used to identify exosomes. Western blot, siRNA transfection, enzyme-linked immunosorbent assay, qRT-PCR, cell viability detection, mouse xenograft tumor models, and immunohistochemical staining were performed to study the function of ABS-induced exosomal EGFR in cell proliferation. Results We found that ABS improved the exosomal EGFR level of normal human esophageal epithelial cells, BE cells, and BE-associated adenocarcinoma cells. The results were confirmed in the serum-derived exosomes from healthy persons and patients suffering from GERD, BE with or without GERD, and EAC with or without GERD. Moreover, cell line-derived exosomal EGFR was found to promote macrophage M2 polarization through the PI3K-AKT pathway. The co-incubation medium of macrophages and exosomes improved cell proliferation and tumor growth, which depended on the exosomal EGFR level. CCL18 was identified as the most effective component of the co-incubation medium to promote EAC cell proliferation by binding to its receptor PITPNM3 in vitro and in vivo. Conclusion Our findings demonstrate that ABS-induced exosomal EGFR regulates macrophage M2 polarization to promote EAC proliferation. This study provides an important insight into the role of ABS in EAC development.

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“…Human papilloma virus (HPV) is a known cause of human cancer, and has been shown to be associated with multiple sites of human cancer, such as cervix, reproductive tract, skin, head and neck, oropharynx and other sites ( Szymonowicz & Chen, 2020 ; De Martel et al, 2017 ; Serup-Hansen et al, 2014 ; Corredor et al, 2022 ). The latest research shows that HPV infection plays a key role in the occurrence and development of Lung carcinoma (LA), especially in non small cell lung carcinoma (NSCLC) ( Zhou et al, 2022 ). High risk human papillomavirus (HR-HPV) will produce HPV oncoproteins E6 and E7 after infecting cells.…”

Section: Introductionmentioning

confidence: 99%

Effects of high-risk human papillomavirus infection on P53, pRb, and survivin in lung adenocarcinoma—a retrospective study

Sun

Yang

Cao

et al. 2023

PeerJ

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Objective To observe the effects of high-risk human papillomavirus (HR-HPV) infection on P53, pRb, and survivin in lung adenocarcinoma (LUAD). Methods The cancerous and cancer-adjacent tissues of 102 patients with LUAD from January 2020 to April 2022 were selected for the study. HR-HPV infection was detected by flow fluorescence method, and P53, pRb, and survivin protein expression was detected by immunohistochemical staining method. Statistical analysis was performed to determine the differences in the HR-HPV infection and the expression of P53, pRb, and survivin proteins between LUAD tissues and cancer-adjacent tissues; the correlation between HR-HPV infection and P53, pRb, and survivin protein expression in cancer tissues; and the correlation between HR-HPV infection and clinicopathological features of LUAD. Results The infection rate of HR-HPV was higher in the LUAD tissues (28.43%) than in cancer-adjacent tissues (7.84%), and the difference was statistically significant (P < 0.05). The positive rates of P53 and survivin protein were higher in the LUAD group (33.33% and 67.16%, respectively) than in the cancer-adjacent group (3.92% and 11.73%, respectively), and the difference was statistically significant (P < 0.05). The positive rate of pRb protein was lower in the LUAD group (58.82%) than in the cancer-adjacent group (92.14%), and the difference was statistically significant (P < 0.05). The positive rates of P53 and survivin proteins were significantly higher in the HR-HPV LUAD group (58.62% and 86.21%, respectively) than in the non-HR-HPV LUAD group (41.38% and 67.12%, respectively), and the difference was statistically significant (P < 0.05). The expression rate of pRb protein was significantly lower in the HR-HPV LUAD group (37.93%) than in the non-HR-HPV LUAD group (67.12%), and the difference was statistically significant (P < 0.05). The expression of p53 and survivin protein was positively correlated with HR-HPV infection (r = 0.338 and 0.444, P < 0.05), whereas the expression of pRb protein was negatively correlated with HR-HPV infection (r = − 0.268, P < 0.05). HR-HPV infection was not associated with gender, age, and smoking in patients with LUAD (P > 0.05). HR-HPV infection was associated with lymph node metastasis and clinical stage of LUAD (P < 0.05). Conclusions HR-HPV infection was associated with lymph node metastasis and clinical stage of LUAD, which may be achieved by up-regulating p53 and survivin protein expression and down-regulating pRb protein expression.

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Exosomal epidermal growth factor receptor is involved in HPV-16 E7-induced epithelial-mesenchymal transition of non-small cell lung cancer cells: A driver of signaling in vivo

Cited by 6 publications

References 57 publications

Dark under the Lamp: Neglected Biological Pollutants in the Environment Are Closely Linked to Lung Cancer

Dark under the Lamp: Neglected Biological Pollutants in the Environment Are Closely Linked to Lung Cancer

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Effects of high-risk human papillomavirus infection on P53, pRb, and survivin in lung adenocarcinoma—a retrospective study

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