IL‐6 expression promoted by Poly(I:C) in cervical cancer cells regulates cytokine expression and recruitment of macrophages

Liu, Xin; Liu, Meng; Chen, Ling; Liang, Ying; Wang, Bingyu; Shao, Qianqian; Wang, Huayang; Yang, Xinggang

doi:10.1111/jcmm.14911

Cited by 19 publications

(8 citation statements)

References 33 publications

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“…Previous studies reported that tumor cells could produce numerous chemokines to attract macrophages, which further dictate the fate of tumor developing and progression through secreting an assorted array of cytokines. It is well-established that IL6 is an essential chemokine for the recruitment of macrophages in cancers (30, 32), such as cervical cancer and prostate cancer. Accordingly, we further evaluated whether HSPB1 could modulate the infiltration of macrophage in breast cancer.…”

Section: Resultsmentioning

confidence: 99%

HSPB1 facilitates chemoresistance through inhibiting ferroptotic cancer cell death and regulating NF-κB signaling pathway in breast cancer

Liang

Wang

Zhang

et al. 2022

Preprint

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Chemoresistance is one of the major causes of therapeutic failure and poor prognosis for breast cancer patients, especially for triple-negative breast cancer patients. However, the underlying mechanism remains elusive. Here, we identified novel functional roles of heat shock protein beta-1 (HSPB1), regulating the chemoresistance and ferroptotic cell death in breast cancer. Based on TCGA and GEO databases, HSPB1 expression was upregulated in breast cancer tissues and associated with poor prognosis of breast cancer patients, which was considered as an independent prognostic factor for breast cancer. Functional assays revealed that HSPB1 could promote cancer growth and metastasis in vitro and in vivo. Furthermore, HSPB1 facilitated doxorubicin resistance through protecting breast cancer cells from drug-induced ferroptosis. Mechanistically, HSPB1 could bind with Ikβ-α and promote its ubiquitination-mediated degradation, leading to increased nuclear translocation and activation of NF-κB signaling. In addition, HSPB1 overexpression led to enhanced secretion of IL6, which further facilitated breast cancer progression. These findings revealed that HSPB1 upregulation might be a key driver to progression and chemoresistance through regulating ferroptosis in breast cancer, while targeting HSPB1 could be an effective strategy against breast cancer.

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Section: Resultsmentioning

confidence: 99%

HSPB1 facilitates chemoresistance through inhibiting ferroptotic cancer cell death and regulating NF-κB signaling pathway in breast cancer

Liang

Wang

Zhang

et al. 2022

Preprint

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“…Dysfunction of the antitumor immune system is closely related to CC development and progression ( Chen Z. et al, 2019 ; Liu J. J. et al, 2020 ; Liu X. et al, 2020 ). High levels of activated memory CD4+T cells predict a better prognosis in patients with CC ( Wang et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Construction of a Six-Gene Prognostic Risk Model Related to Hypoxia and Angiogenesis for Cervical Cancer

Liu

Zhu²,

Wang

et al. 2022

Front. Genet.

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Background: The prognosis of cervical cancer (CC) is poor and not accurately reflected by the primary tumor node metastasis staging system. Our study aimed to develop a novel survival-prediction model.Methods: Hallmarks of CC were quantified using single-sample gene set enrichment analysis and univariate Cox proportional hazards analysis. We linked gene expression, hypoxia, and angiogenesis using weighted gene co-expression network analysis (WGCNA). Univariate and multivariate Cox regression was combined with the random forest algorithm to construct a prognostic model. We further evaluated the survival predictive power of the gene signature using Kaplan-Meier analysis and receiver operating characteristic (ROC) curves.Results: Hypoxia and angiogenesis were the leading risk factors contributing to poor overall survival (OS) of patients with CC. We identified 109 candidate genes using WGCNA and univariate Cox regression. Our established prognostic model contained six genes (MOCSI, PPP1R14A, ESM1, DES, ITGA5, and SERPINF1). Kaplan-Meier analysis indicated that high-risk patients had worse OS (hazard ratio = 4.63, p < 0.001). Our model had high predictive power according to the ROC curve. The C-index indicated that the risk score was a better predictor of survival than other clinicopathological variables. Additionally, univariate and multivariate Cox regressions indicated that the risk score was the only independent risk factor for poor OS. The risk score was also an independent predictor in the validation set (GSE52903). Bivariate survival prediction suggested that patients exhibited poor prognosis if they had high z-scores for hypoxia or angiogenesis and high risk scores.Conclusions: We established a six-gene survival prediction model associated with hypoxia and angiogenesis. This novel model accurately predicts survival and also provides potential therapeutic targets.

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“…Thus, the interplay between HPV-infected host cells and the local CVM may determine the course of cervical carcinogenesis. The microbiome in the local CVM can modulate immune responses, including critical components of antitumor immunity, thereby contributing to the therapeutic activity of immune checkpoint inhibitors ( 12 ). However, crosstalk between the local vaginal microbiome and the CVM during cervical carcinogenesis remains controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the degradation of innate defenses may occur ( 5, 25 ). In addition, persistent chronic inflammation may lead to anti-inflammatory effects and regulate the expression of cytokines, such as IL6, which may increase the risk of cytologic abnormalities ( 12 ). In previous research by the authors of the current study, it was observed that chronic inflammation (graded by inflammatory cell count) significantly increased the risk of cytologic abnormalities ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Bacterial Vaginosis Decreases the Risk of Cervical Cytological Abnormalities

Long

Zhang

et al. 2022

Cancer Prevention Research

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Genital tract infections, including vulvovaginal candidiasis (VVC) and bacterial vaginosis (BV), have emerged as potential modulators of persistent human papillomavirus (HPV) infections causing cervical cytological abnormalities (CA) and cervical cancer. This study aimed to investigate whether VVC or BV had an additional effect on HPV infection and thus caused such abnormalities. ThinPrep cytological tests were used to detect CA, VVC, and BV in 14,679 women. Cytological abnormalities included atypical squamous cells of undetermined significance (ASC-US), low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), atypical squamous cells-cannot exclude HSIL (ASC-H), and squamous cell carcinoma (SCC). Logistic regression Model 1 (univariate regression) and Model 2 (multivariate logistic regression analysis adjusted for age combined with HPV infection) were used to analyze the association between BV and CA, or VVC and CA, alone or in the presence of HPV infection. BV infection rates were found to be significantly higher in the cytology-negative group among all participants and those with HPV infection (p=0.003, p<0.001, respectively). Analyses using Model 1 and Model 2 both pointed to BV as a protective factor against CA for all participants (OR=0.36, 0.17, respectively, p<0.05) and for HPV-infected participants (OR=0.17, 0.16, respectively, p<0.05). Neither VVC nor VVC + HPV was significantly associated with the incidence of CA based on Model 1 (OR=0.94, 0.71, respectively, p>0.05) and Model 2 (OR=0.91, 0.74, respectively, p>0.05). Furthermore, neither VVC nor BV increased the incidence of CA regardless of HPV infection status, while BV might possibly prevent CA in women co-infected by HPV.

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IL‐6 expression promoted by Poly(I:C) in cervical cancer cells regulates cytokine expression and recruitment of macrophages

Cited by 19 publications

References 33 publications

HSPB1 facilitates chemoresistance through inhibiting ferroptotic cancer cell death and regulating NF-κB signaling pathway in breast cancer

HSPB1 facilitates chemoresistance through inhibiting ferroptotic cancer cell death and regulating NF-κB signaling pathway in breast cancer

Construction of a Six-Gene Prognostic Risk Model Related to Hypoxia and Angiogenesis for Cervical Cancer

Bacterial Vaginosis Decreases the Risk of Cervical Cytological Abnormalities

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