Synthesis of Polyphenon-60 Functionalized Bimetallic Ag–Pt Nanostructures that Inhibit Proliferation of SiHa Cells

Purpose: The current study was intended to research the functional role and regulatory mechanism of microRNA-96-5p in the progression of cervical cancer. Methods: MicroRNA-96-5p expression in cervical cancer tissues was assessed by quantitative real-time polymerase chain reaction. The association between microRNA-96-5p expression and clinicopathological features of patients with cervical cancer was analyzed. MTT, flow cytometry, wound healing, and transwell assay were performed to evaluate the viability, apoptosis, migration, and invasion of Hela and SiHa cells. Targetscan, dual-luciferase reporter gene assay, and RNA pull-down analysis were constructed to evaluate the target relationship between microRNA-96-5p and secreted frizzled-related protein 4. Results: MicroRNA-96-5p was overexpressed in cervical cancer tissues, and microRNA-96-5p expression was markedly associated with the clinical stage and lymph node metastasis of patients with cervical cancer. Overexpressed microRNA-96-5p facilitated the viability, migration, invasion, and inhibited the apoptosis of Hela and SiHa cells, whereas suppression of microRNA-96-5p exerted the opposite trend. Secreted frizzled-related protein 4 was proved to be a target of microRNA-96-5p. Silencing of secreted frizzled-related protein 4 eliminated the anti-tumor effect of microRNA-96-5p on cervical cancer cells. Conclusions: MicroRNA-96-5p facilitated the viability, migration, and invasion and inhibited the apoptosis of cervical cancer cells via negatively regulating secreted frizzled-related protein 4.

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Influence of icariin on inflammation, apoptosis, invasion, and tumor immunity in cervical cancer by reducing the TLR4/MyD88/NF-κB and Wnt/β-catenin pathways

Cancer Cell International ◽

10.1186/s12935-021-01910-2 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Chunyang Li ◽

Shuangqing Yang ◽

Huaqing Ma ◽

Mengjia Ruan ◽

Luyan Fang ◽

...

Keyword(s):

Cervical Cancer ◽

Underlying Mechanism ◽

Tissue Growth ◽

Migration And Invasion ◽

Dependent Manner ◽

Antitumor Effects ◽

Siha Cells ◽

Cervical Cancer Cells

Abstract Background Cervical cancer is a type of the most common gynecology tumor in women of the whole world. Accumulating data have shown that icariin (ICA), a natural compound, has anti-cancer activity in different cancers, including cervical cancer. The study aimed to reveal the antitumor effects and the possible underlying mechanism of ICA in U14 tumor-bearing mice and SiHa cells. Methods The antitumor effects of ICA were investigated in vivo and in vitro. The expression of TLR4/MyD88/NF-κB and Wnt/β-catenin signaling pathways were evaluated. Results We found that ICA significantly suppressed tumor tissue growth and SiHa cells viability in a dose-dependent manner. Also, ICA enhanced the anti-tumor humoral immunity in vivo. Moreover, ICA significantly improved the composition of the microbiota in mice models. Additionally, the results clarified that ICA significantly inhibited the migration, invasion capacity, and expression levels of TGF-β1, TNF-α, IL-6, IL-17A, IL-10 in SiHa cells. Meanwhile, ICA was revealed to promote the apoptosis of cervical cancer cells by down-regulating Ki67, survivin, Bcl-2, c-Myc, and up-regulating P16, P53, Bax levels in vivo and in vitro. For the part of mechanism exploration, we showed that ICA inhibits the inflammation, proliferation, migration, and invasion, as well as promotes apoptosis and immunity in cervical cancer through impairment of TLR4/MyD88/NF-κB and Wnt/β-catenin pathways. Conclusions Taken together, ICA could be a potential supplementary agent for cervical cancer treatment.

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Clinacanthus nutans standardized fraction arrested SiHa cells at G1/S and induced apoptosis via upregulation of p53

Journal of Pharmacy And Bioallied Sciences ◽

10.4103/jpbs.jpbs_262_19 ◽

2020 ◽

Vol 12 (6) ◽

pp. 768

Author(s):

Yusmazura Zakaria ◽

NikAina Syazana Nik Zainuddin ◽

Hussin Muhammad ◽

NikFakhuruddin Nik Hassan ◽

NorHayati Othman

Keyword(s):

Siha Cells ◽

Clinacanthus Nutans ◽

Induced Apoptosis

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Cellular Levels of Oxidative Stress Affect the Response of Cervical Cancer Cells to Chemotherapeutic Agents

BioMed Research International ◽

10.1155/2014/574659 ◽

2014 ◽

Vol 2014 ◽

pp. 1-14 ◽

Cited By ~ 23

Author(s):

Maria Filippova ◽

Valery Filippov ◽

Vonetta M. Williams ◽

Kangling Zhang ◽

Anatolii Kokoza ◽

...

Keyword(s):

Oxidative Stress ◽

Cervical Cancer ◽

Cancer Cells ◽

Adaptive Systems ◽

Chemotherapeutic Agents ◽

Rt Pcr ◽

Cellular Models ◽

Siha Cells ◽

Ros Metabolism ◽

Cervical Cancer Cells

Treatment of advanced and relapsed cervical cancer is frequently ineffective, due in large part to chemoresistance. To examine the pathways responsible, we employed the cervical carcinoma-derived SiHa and CaSki cells as cellular models of resistance and sensitivity, respectively, to treatment with chemotherapeutic agents, doxorubicin, and cisplatin. We compared the proteomic profiles of SiHa and CaSki cells and identified pathways with the potential to contribute to the differential response. We then extended these findings by comparing the expression level of genes involved in reactive oxygen species (ROS) metabolism through the use of a RT-PCR array. The analyses demonstrated that the resistant SiHa cells expressed higher levels of antioxidant enzymes. Decreasing or increasing oxidative stress led to protection or sensitization, respectively, in both cell lines, supporting the idea that cellular levels of oxidative stress affect responsiveness to treatment. Interestingly, doxorubicin and cisplatin induced different profiles of ROS, and these differences appear to contribute to the sensitivity to treatment displayed by cervical cancer cells. Overall, our findings demonstrate that cervical cancer cells display variable profiles with respect to their redox-generating and -adaptive systems, and that these different profiles have the potential to contribute to their responses to treatments with chemotherapy.

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Trichomonas Vaginalis Induces Apoptosis via ROS and ER Stress Through ER-mitochondria Crosstalk in Human Cervical Epithelial Cells

10.21203/rs.3.rs-330817/v1 ◽

2021 ◽

Author(s):

Fei Fei Gao ◽

Juan-Hua Quan ◽

Min A Lee ◽

Wei Ye ◽

Jae-Min Yuk ◽

...

Keyword(s):

Stress Response ◽

Epithelial Cells ◽

Er Stress ◽

Mitochondrial Dysfunction ◽

Parasite Burden ◽

Dependent Manner ◽

Ros Production ◽

Er Stress Response ◽

Siha Cells ◽

Mitochondrial Ros

Abstract Background: Human trichomoniasis is one of the most common sexually transmitted infections; however, its pathogenesis remains unclear. Here, we investigated the role of the endoplasmic reticulum (ER) in apoptosis induction by T. vaginalis in human cervical epithelial SiHa cellsMethods: We evaluated the cytotoxicity, apoptosis, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), ER stress response, and Bcl-2 family protein expressions using LDH assay, immunocytochemistry, flow cytometry, JC-1 dye staining, and western blotting.Results: T. vaginalis induced LDH-dependent cytotoxicity, mitochondrial ROS production, and apoptosis in SiHa cells, parasite burden- and infection time-dependently. T. vaginalis also induced ER stress response and mitochondrial dysfunction, such as MMP depolarization and imbalance in levels of Bcl-2 family proteins, in SiHa cells in a parasite burden- and infection time-dependent manner. Pretreatment with N-Acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA, ER stress inhibitor) significantly alleviated apoptosis, ROS production, mitochondrial dysfunction, and ER stress response in a dose-dependent manner. These data suggested that SiHa cell apoptosis is affected by ROS and ER stress after T. gondii infection. In addition, T. vaginalis induced ASK1 and JNK phosphorylation in SiHa cells, however 4-PBA or SP600125 (JNK inhibitor) pretreatment significantly attenuated ASK1/JNK phosphorylation, mitochondrial dysfunction, apoptosis, and ER stress response in SiHa cells, dose-dependently.Conclusions: T. vaginalis induces mitochondrial apoptosis via ROS and parasite-mediated ER stress via the IRE1/ASK1/JNK/Mcl-1 pathways, and also induces ER stress response directly and mitochondrial ROS-dependently in human cervical epithelial SiHa cells, thus, T. vaginalis induces apoptosis via ROS and ER stress through ER-mitochondria crosstalk in human cervical epithelial cells. These results expand our understanding of the molecular mechanisms underlying the pathogenesis of human trichomoniasis.

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Non-contact co-culture with human vascular endothelial cells promotes epithelial-to-mesenchymal transition of cervical cancer SiHa cells by activating the NOTCH1/LOX/SNAIL pathway

Cellular & Molecular Biology Letters ◽

10.1186/s11658-019-0163-z ◽

2019 ◽

Vol 24 (1) ◽

Cited By ~ 3

Author(s):

Jinghua Ou ◽

Defeng Guan ◽

Yongxiu Yang

Keyword(s):

Cervical Cancer ◽

Endothelial Cells ◽

Epithelial To Mesenchymal Transition ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Mesenchymal Transition ◽

Siha Cells

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Adherence of Trichomonas vaginalis to SiHa Cells is Inhibited by Diphenyleneiodonium

Microorganisms ◽

10.3390/microorganisms8101570 ◽

2020 ◽

Vol 8 (10) ◽

pp. 1570

Author(s):

Yeeun Kim ◽

Young Ha Lee ◽

In-Wook Choi ◽

Bu Yeon Heo ◽

Ju-Gyeong Kang ◽

...

Keyword(s):

Flow Cytometry ◽

Trichomonas Vaginalis ◽

Parasitic Infection ◽

Oxidase Inhibitor ◽

Host Cells ◽

Epithelial Cell Line ◽

Dependent Manner ◽

Siha Cells ◽

Parasite Infections

Microbial adhesion is critical for parasitic infection and colonization of host cells. To study the host–parasite interaction in vitro, we established a flow cytometry-based assay to measure the adherence of Trichomonas vaginalis to epithelial cell line SiHa. SiHa cells and T. vaginalis were detected as clearly separated, quantifiable populations by flow cytometry. We found that T. vaginalis attached to SiHa cells as early as 30 min after infection and the binding remained stable up to several hours, allowing for analysis of drug treatment efficacy. Importantly, NADPH oxidase inhibitor DPI treatment induced the detachment of T. vaginalis from SiHa cells in a dose-dependent manner without affecting host cell viability. Thus, this study may provide an understanding for the potential development of therapies against T. vaginalis and other parasite infections.

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