Withdrawal Notice: Zinc Finger Nuclease Combines with Cisplatin and Trichostatin A Enhances the Antitumor Potency in Cervical Cancer Cells

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The Antitumor Efficiency of Zinc Finger Nuclease Combined with Cisplatin and Trichostatin A in Cervical Cancer Cells

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520620666200804102300 ◽

2020 ◽

Vol 20 (17) ◽

pp. 2125-2135

Author(s):

Ci Ren ◽

Chun Gao ◽

Xiaomin Li ◽

Jinfeng Xiong ◽

Hui Shen ◽

...

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Zinc Finger ◽

Hela Cells ◽

Colony Formation ◽

Trichostatin A ◽

Combined Therapy ◽

Hpv E7 ◽

Anti Cancer ◽

Cervical Cancer Cells

Background: Persistent infection with the high-risk of human papillomavirus (HR-HPVs) is the primary etiological factor of cervical cancer; HR-HPVs express oncoproteins E6 and E7, both of which play key roles in the progression of cervical carcinogenesis. Zinc Finger Nucleases (ZFNs) targeting HPV E7 induce specific shear of the E7 gene, weakening the malignant biological effects, hence showing great potential for clinical transformation. Objective: Our aim was to develop a new comprehensive therapy for better clinical application of ZFNs. We here explored the anti-cancer efficiency of HPV targeted ZFNs combined with a platinum-based antineoplastic drug Cisplatin (DDP) and an HDAC inhibitor Trichostatin A (TSA). Methods: SiHa and HeLa cells were exposed to different concentrations of DDP and TSA; the appropriate concentrations for the following experiments were screened according to cell apoptosis. Then cells were grouped for combined or separate treatments; apoptosis, cell viability and proliferation ability were measured by flow cytometry detection, CCK-8 assays and colony formation assays. The xenograft experiments were also performed to determine the anti-cancer effects of the combined therapy. In addition, the HPV E7 and RB1 expressions were measured by western blot analysis. Results: Results showed that the combined therapy induced about two times more apoptosis than that of ZFNs alone in SiHa and HeLa cells, and much more inhibition of cell viability than either of the separate treatment. The colony formation ability was inhibited more than 80% by the co-treatment, the protein expression of HPV16/18E7 was down regulated and that of RB1 was elevated. In addition, the xenografts experiment showed a synergistic effect between DDP and TSA together with ZFNs. Conclusion: Our results demonstrated that ZFNs combined with DDP or TSA functioned effectively in cervical cancer cells, and it provided novel ideas for the prevention and treatment of HPV-related cervical malignancies.

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Mechanisms and Applications of the Anti-cancer Effect of Pharmacological Ascorbic Acid in Cervical Cancer Cells

Frontiers in Oncology ◽

10.3389/fonc.2020.01483 ◽

2020 ◽

Vol 10 ◽

Author(s):

Tsai-Ming Wu ◽

Shu-Ting Liu ◽

Ssu-Yu Chen ◽

Gunng-Shinng Chen ◽

Chia-Chun Wu ◽

...

Keyword(s):

Cervical Cancer ◽

Ascorbic Acid ◽

Cancer Cells ◽

Anti Cancer ◽

Cervical Cancer Cells

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Proteomic analysis of anti-cancer effects by paclitaxel treatment in cervical cancer cells

Gynecologic Oncology ◽

10.1016/j.ygyno.2005.04.010 ◽

2005 ◽

Vol 98 (1) ◽

pp. 45-53 ◽

Cited By ~ 46

Author(s):

Keun-Ho Lee ◽

Eun-Kyoung Yim ◽

Chan-Joo Kim ◽

Sung-Eun Namkoong ◽

Soo-Jong Um ◽

...

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Proteomic Analysis ◽

Anti Cancer ◽

Cervical Cancer Cells ◽

Paclitaxel Treatment

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Essential Oil from Zingiber ottensii Induces Human Cervical Cancer Cell Apoptosis and Inhibits MAPK and PI3K/AKT Signaling Cascades

Plants ◽

10.3390/plants10071419 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1419

Author(s):

Jirapak Ruttanapattanakul ◽

Nitwara Wikan ◽

Kittinan Chinda ◽

Thanathorn Jearanaikulvanich ◽

Napatsorn Krisanuruks ◽

...

Keyword(s):

Cervical Cancer ◽

Essential Oil ◽

Western Blot ◽

Cancer Cells ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Growth And Survival ◽

Anti Cancer ◽

Cervical Cancer Cells ◽

Human Cervical Cancer

Zingiber ottensii (ZO) is a local plant in Thailand and has been used as a Thai traditional therapy for many conditions. ZO has been reported to exhibit many pharmacological effects, including anti-cancer activity. Nevertheless, its anti-cancer effects explored at the signaling level have not been elucidated in cervical cancer, which is one of the leading causes of fatality in females. We discovered that the essential oil of ZO significantly increased the apoptosis of human cervical cancer cells (HeLa) after 24 h of treatment in a concentration-dependent manner. Our data also clearly demonstrated that ZO essential oil reduced IL-6 levels in the culture supernatants of the cancer cells. Moreover, Western blot analysis clearly verified that cells were induced to undergo apoptotic death via caspase activation upon treatment with ZO essential oil. Interestingly, immunofluorescence studies and Western blot analyses showed that ZO essential oil suppressed epidermal growth factor (EGF)-induced pAkt and pERK1/2 signaling pathway activation. Together, our study demonstrates that ZO essential oil can reduce the proliferation and survival signaling of HeLa cervical cancer cells. Our study provides convincing data that ZO essential oil suppresses the growth and survival of cervical cancer cells, and it may be a potential choice for developing an anti-cancer agent for treating certain cervical cancers.

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Kaempferia parviflora Extract Inhibits STAT3 Activation and Interleukin-6 Production in HeLa Cervical Cancer Cells

International Journal of Molecular Sciences ◽

10.3390/ijms20174226 ◽

2019 ◽

Vol 20 (17) ◽

pp. 4226 ◽

Cited By ~ 3

Author(s):

Benjamart Suradej ◽

Siriwoot Sookkhee ◽

Jukreera Panyakaew ◽

Pitchaya Mungkornasawakul ◽

Nitwara Wikan ◽

...

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Egf Receptor ◽

Kaempferia Parviflora ◽

Ki 67 ◽

Cellular Marker ◽

Anti Cancer ◽

Cell Progression ◽

Cervical Cancer Cells ◽

Cancer Agent

Kaempferia parviflora (KP) has been reported to have anti-cancer activities. We previously reported its effects against cervical cancer cells and continued to elucidate the effects of KP on inhibiting the production and secretion of interleukin (IL)-6, as well as its relevant signaling pathways involved in cervical tumorigenesis. We discovered that KP suppressed epidermal growth factor (EGF)-induced IL-6 secretion in HeLa cells, and it was associated with a reduced level of Glycoprotein 130 (GP130), phosphorylated signal transducers and activators of transcription 3 (STAT3), and Mcl-1. Our data clearly showed that KP has no effect on nuclear factor kappa B (NF-κB) localization status. However, we found that KP inhibited EGF-stimulated phosphorylation of tyrosine 1045 and tyrosine 1068 of EGF receptor (EGFR) without affecting its expression level. The inhibition of EGFR activation was verified by the observation that KP significantly suppressed a major downstream MAP kinase, ERK1/2. Consistently, KP reduced the expression of Ki-67 protein, which is a cellular marker for proliferation. Moreover, KP potently inhibited phosphorylation of STAT3, Akt, and the expression of Mcl-1 in response to exogenous IL-6 stimulation. These data suggest that KP suppresses EGF-induced production of IL-6 and inhibits its autocrine IL-6/STAT3 signaling critical for maintaining cancer cell progression. We believe that KP may be a potential alternative anti-cancer agent for suppressing cervical tumorigenesis.

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