The Expression of Toll-like Receptor 8 and Its Relationship with VEGF and Bcl-2 in Cervical Cancer

Zhang, Yun; Yang, Heng; Barnie, Prince Amoah; Yang, Ping; Su, Zhaoliang; Chen, Jian Guo; Jiao, Zhijun; Lu, Liwei; Wang, Shengjun; Xu, Huaxi

doi:10.7150/ijms.8428

Cited by 34 publications

(29 citation statements)

References 23 publications

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“…Bcl-2 promotes the proliferation of cancer cells (16,17). In addition, Bcl-2 is overexpressed in cervical cancer cells and is closely correlated with the development and progression of cervical cancer (18). Bax belongs to the Bcl-2 family and forms dimers with Bcl-2 to regulate the balance between cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells

Cao

Meng

2017

Molecular Medicine Reports

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The present study aimed to investigate the role and the molecular mechanisms underlying the effects of microRNA-21 (miR-21) on the proliferation, apoptosis and colony formation of cervical cancer cells, and to examine the role of miR-21 in mediating the sensitivity of cervical cancer cells to paclitaxel (PTX). Reverse transcription‑quantitative polymerase chain reaction was employed to determine the level of miR‑21 in various cervical cancer and normal cervical cells. The results revealed that the expression levels of miR-21 in cervical cancer cells were markedly higher when compared with normal cervical cells. Subsequently, a miR‑21 inhibitor or negative control (NC) was transfected into cervical cancer cells. Cell viability, colony formation and apoptosis were then analyzed using an MTT assay, crystal violet and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression level of B-cell lymphoma‑2 (Bcl‑2), Bcl‑2‑associated X (Bax), programmed cell death 4 (PDCD4), survivin, c‑myc, phosphatase and tensin homolog (PTEN) and phosphorylated (p)‑AKT were determined by western blot analysis. The sensitivity of cervical cancer cells to PTX (25, 50 and 100 µg/ml) was characterized using an MTT assay. The results demonstrated that the miR-21 inhibitor promoted apoptosis of cervical cancer cells and suppressed their proliferation and colony formation when compared with the NC. In addition, the expression levels of Bcl‑2, survivin, c‑myc and p‑AKT were significantly downregulated in cells transfected with the miR‑21 inhibitor, whilst the expression levels of Bax, PDCD4 and PTEN were significantly upregulated. Furthermore, the miR‑21 inhibitor significantly enhanced the inhibition efficacy of PTX at a range of concentrations in cervical cancer cells. It was concluded that inhibition of miR‑21 suppressed cell proliferation and colony formation through regulating the PTEN/AKT pathway, and improved PTX sensitivity in cervical cancer cells. The results of the present study may contribute to the development of miRNA‑based cervical cancer therapy in the future.

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Section: Discussionmentioning

confidence: 99%

miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells

Cao

Meng

2017

Molecular Medicine Reports

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“…These molecules activate specific TLRs, leading to further chronic inflammation, which is one of the main cancer-promoting factors (28). The expression of TLRs in the tumor microenviroment directly influences tumor development and its interactions with the immune system (38). The activation of TLRs upregulates pro-oncogenic pathways via the induction of nitric oxide synthase and cyclooxygenase 2, which regulate the expression of TLRs and promote a positive feedback mechanism, thus leading to the progression of cancer and the development of more aggressive neoplastic phenotypes (38).…”

Section: Resultsmentioning

confidence: 99%

“…TLRs are also capable of recognizing molecular patterns that are typical of endogenous cellular damage (DAMPs), and are thus implicated in processes of cellular proliferation and survival, apoptosis, angiogenesis and tissue remodelling (36). TLRs are expressed by immune cells and other cellular types, including cancer cells (37,38). Significant quantities of DAMPs are released in the tumor microenviroment by damaged epithelial cells and necrotic tumor cells (28).…”

Section: Resultsmentioning

confidence: 99%

TLR7 Gln11Leu single nucleotide polymorphism and susceptibility to cutaneous melanoma

et al. 2016

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Abstract. Cutaneous melanoma is a life-threatening skin cancer. Its incidence is rapidly increasing, and early diagnosis is the main factor able to improve its poor prognosis. Toll-like receptors (TLRs) are transmembrane glycoproteins that recognize pathogen-and damage-associated molecular patterns, against which TLRs activate the innate immune response and initiate the adaptive immune response. Genetic variations of these receptors may alter the immune system, and are involved in evolution and susceptibility to various diseases, including cancer. The aim of the present study was to evaluate whether the presence of TLR7 glutamine (Gln) 11 leucine (Leu) polymorphism confers an increased susceptibility to cutaneous melanoma. For that purpose, a case-control study was performed with 182 melanoma cases and 89 controls. To highlight the possible association between the aforementioned polymorphism and the susceptibility to melanoma, 93 cases of single melanoma and 89 cases of multiple primary melanoma (MPM) were compared in the present study. Since the TLR7 gene is localized on the chromosome X, the allelic frequency of the Gln11Leu polymorphism was analyzed separately in males and females. The distribution of allele frequencies between melanoma cases and controls (P=0.245) and between single melanoma and MPM cases (P=0.482) was not significant. Therefore, the present results do not suggest an association between TLR7 Gln11Leu polymorphism and susceptibility to cutaneous melanoma. Further studies are required to analyze the influence of other TLR polymorphisms on the susceptibility to malignant melanoma and the involvement of innate immunity in this malignancy.

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“…In contrast to TLR9, the TLR3/5/8 pathways are activated in hrHPV-infected KCs. High expression levels of TLR8 in cervical cancer cells are associated with the upregulated expression of B-cell lymphoma-2 and vascular endothelial growth factor in these cells (27). A previous study found that there is marked TLR4 expression in hrHPV-positive cells and that its expression is associated with the virus type, as well as the histopathological grade.…”

Section: Hpv Infection Regulating the Host Immune Responsementioning

confidence: 99%

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

et al. 2015

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Abstract. Human papillomavirus (HPV) is widely known as a cause of cervical intraepithelial neoplasia (CIN) and cervical cancer. The mechanisms involved have been studied by numerous studies. The integration of the virus genome into the host cells results in the abnormal regulation of cell cycle control. HPV can also induce immune evasion of the infected cells, which enable the virus to be undetectable for long periods of time. The induction of immunotolerance of the host's immune system by the persistent infection of HPV is one of the most important mechanisms for cervical lesions. The present review elaborates on the roles of several types of immune cells, such as macrophages and natural killer cells, which are classified as innate immune cells, and dendritic cells (DCs), cluster of differentiation (CD)4 + /CD8 + T cells and regulatory T cells, which are classified as adaptive immune cells. HPV infection could effect the differentiation of these immune cells in a unique way, resulting in the host's immune tolerance to the infection. The immune system modifications induced by HPV infection include tumor-associated macrophage differentiation, a compromised cellular immune response, an abnormal imbalance between type 1 T-helper cells (Th1) and Th2 cells, regulatory T cell infiltration, and downregulated DC activation and maturation. To date, numerous types of preventative vaccines have been created to slow down carcinogenesis. Immune response activation-based therapeutic vaccine is becoming more and more attractive for the treatment of HPV-associated diseases.

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The Expression of Toll-like Receptor 8 and Its Relationship with VEGF and Bcl-2 in Cervical Cancer

Cited by 34 publications

References 23 publications

miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells

miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells

TLR7 Gln11Leu single nucleotide polymorphism and susceptibility to cutaneous melanoma

Effect of human papillomavirus infection on the immune system and its role in the course of cervical cancer

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