Effect of Zanthoxylum acanthopodium methanol extract on CDK4 expression to cervical cancer

Author(s):  
Syafruddin Ilyas ◽  
Rostime H. Simanullang ◽  
Salomo Hutahaean ◽  
Rosidah Rosidah ◽  
Putri C. Situmorang

Cervical cancer is a disease from the Human papillomavirus (HPV) through transmission, virus persistence, clone development until infecting the cells in the cervical. This study is to determine CDK4 expression in cervical cancer cells after being given Zanthoxylum acanthopodium methanol extract (ZAM) and the histological description of cervical cancer cells. This study consisted of 5 treatment groups. K-: control group, K+: rats model of cancer, P1: rats model of cancer with a dose of 100mg/BW of ZAM, P2: rats model of cancer with a dose of 200 mg/BW of ZAM, and P3: rats model of cancer with a dose of 400 mg/BW of ZAM. The cervical tissue was prepared on paraffin blocks and given Immunohistochemistry staining. Results showed that the expression of CDK4 are reduced in the ZAM treatment at doses of 200 and 400mg/KgBW (P<0.05) in cervical histology, but in doses of 100mg/kg BW, many brown marks are still visible on the cervical tissue. These proteins will bind, inhibit proteins, cell cycle development, modulate cell division, and signal transduction pathways of apoptotic signaling. The injection of benzopyrene and given ZAM in cervical tissue affect hematological values. ZAM affects and improves cervical histology after benzopyrene injection. The extract of andaliman can be developed into a cervical cancer drug candidate.

2021 ◽  
Vol 13 (8) ◽  
pp. 1506-1511
Author(s):  
Minjuan Xu ◽  
Jun Huang ◽  
Liefeng Wang

Cervical cancer is often treated with surgery, radiotherapy and chemotherapy, but it does not have the advantages of precise treatment and prognosis is not ideal. Molecular targeted therapy can make up for the above shortcomings. This study mainly analyzed the influence of miR-126 on cervical cancer cells and possible molecular mechanisms, so as to provide a reference for better clinical improvement of prognosis for cervical cancer. C33a cells were assigned into control group, empty carrier group (C33a cells were co-cultured with liposome nanoparticle carrier), inhibitor group (C33a cells were treated with PD-1/PD-L1 signaling pathway inhibitor), miR-126 group (miR-126 with liposomal nanoparticles as carrier was added to C33a cells), followed by expression analysis of miR-126 and AK2, cell proliferation, PD-1/PD-L1 signaling and phosphorylation levels, as well as tumor mass and volume in nude mice. At 24 h, no difference of cell proliferation was found (P > 0.05) but cell proliferation showed significant differences after cell growth of 48 h, with lower proliferation in inhibitor group and miR-126 group (P < 0.05). The levels of PD-1, PD-L1, AK2, and p-PD-1 in inhibitor group and miR-126 group were significantly lower than for the other two groups (P > 0.05). There was a target relationship between miR-126 and AK2. The transplanted tumor in the miR-126 group was significantly decreased, with lower tumor mass and volume than control group (P < 0.05). The carrier-based miR-126 and PD-1/PD-L1 signaling inhibitors can inhibit cervical cancer cell proliferation.


Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 1019-1027
Author(s):  
Lijie He ◽  
Jing Wang ◽  
Dandan Chang ◽  
Dandan Lv ◽  
Haina Li ◽  
...  

AbstractObjectiveThis article aims to investigate the effect of miRNA-200b on the proliferation and apoptosis of cervical cancer cells by targeting RhoA.MethodsHeLa cells of cervical cancer were divided into five groups: blank control group, negative control group (miRNA-200b mimic NC), miRNA-200b mimic group, RhoA-negative control group, and RhoA overexpression group. Cells were collected 48 h after transfection. The expression levels of miRNA-200b were detected by RT-PCR. Target relationship between miRNA-200b and RhoA was verified by the dual-luciferase reporter assay. RhoA mRNA and protein expression were detected by western blot and RT-PCR methods. Flow cytometry was used to detect the apoptosis of cells in each group, and the CCK8 method was used to detect the proliferation of cells in each group. The mRNA and protein expression of Bax and cyclin D1 were detected by RT-PCR and western blot.ResultsThe results of the dual luciferase reporter assay showed that RhoA was the target gene of microRNA 200b. Compared with the blank control group and the miRNA-200b mimic-NC group, the proportion of apoptotic cells increased significantly in the miRNA-200b mimic group, and the proliferation of cells was inhibited (P < 0.05). After overexpression of RhoA, the percentage of apoptotic cells decreased and the ability of cell proliferation increased significantly (P < 0.05).ConclusionmiRNA-200b can inhibit the proliferation and promote the apoptosis of cervical cancer cells by targeting the RhoA gene.


2018 ◽  
Vol 2018 ◽  
pp. 1-19 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan ◽  
Lee Chin Chan

Manilkara zapota (L.) P. Royen (family: Sapotaceae) is commonly called sapodilla, or locally known as ciku. The detailed mechanisms underlying Manilkara zapota leaf methanol extract against HeLa human cervical cancer cells have yet to be investigated. Therefore, our present study is designed to investigate the ability to induce apoptosis and the underlying mechanisms of Manilkara zapota leaf methanol extract inducing cytotoxicity in HeLa cells. The apoptotic cell death was assessed using Annexin V-propidium iodide staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential activities were measured using dichlorodihydrofluorescein diacetate and MitoLite Orange, respectively, by NovoCyte Flow Cytometer. Bax and Bcl-2 expression were evaluated using Enzyme-Linked Immunosorbent Assay. Caspase-3 activity was determined using a colorimetric assay. The associated biological interaction pathways were evaluated using quantitative real-time PCR. Our data showed that HeLa cells were relatively more sensitive to Manilkara zapota leaf methanol extract than other cancer cell lines studied. Overall analyses revealed that Manilkara zapota leaf methanol extract can inhibit the viability of HeLa cells, induce mitochondrial ROS generation, and inhibit nuclear factor-kappa B (NF-κB) and epidermal growth factor receptor (EGFR) transcriptional activities. Our results suggested that Manilkara zapota leaf methanol extract might represent a potential anticervical cancer agent.


2020 ◽  
Vol 10 (8) ◽  
pp. 1206-1212
Author(s):  
Yunyan Ma ◽  
LV Xiaoyan ◽  
Xiaojiang Jia ◽  
Jingzhen Zhou ◽  
Zhenbo Ouyang ◽  
...  

High-risk HPV16 is an important factor for cervical cancer. HPV16 E7 can promote the malignant transformation of cervical epithelial cells. Forkhead box protein A1 (FOXA1) is abnormally expressed in several tumors. Our study assessed HPV16 E7's effect on cervical cancer cells. Hela cells were divided into control group; HPV16 E7 group; and siFOXA1+ HPV16 E7 group followed by analysis of HPV16 E7 and FOXA1 expression by Real-time PCR and Western blot, cell proliferation by MTT assay, Caspase 3 activity, Bax and Bcl-2 expression by Real-time PCR as well as cell invasion by Transwell assay. In HPV16 E7 group, HPV16 E7 and HOXA1 expression was significantly increased, cell proliferation was promoted, invasive ability was increased, Caspase 3 activity and Bax expression was decreased, and Bcl-2 expression was increased compared to control group (P < 0 05). Conversely, inhibition of FOXA1 expression in Hela cells overexpressing HPV16 E7 can significantly inhibit cell proliferation and invasion, and promote apoptosis (P < 0 05). HPV16 E7 protein can up-regulate FOXA1 in host cells, and promote cervical cancer cell growth, proliferation and invasion, indicating that it is one of the key factors contributing to cervical cancer.


Author(s):  
Jie Chen ◽  
Lili Ge ◽  
Xiaoyan Shi ◽  
Juan Liu ◽  
Hongjie Ruan ◽  
...  

Background: Increasing evidence shows that GSDME is involved in tumor chemotherapy. Lobaplatin is an important chemotherapy drug for the treatment of cervical cancer. However, the exact mechanism of lobaplatin in the treatment of cervical cancer remains unclear. Objective: In this study, we study whether GSDME is a new mechanism of lobaplatin in the treatment of cervical cancer. Methods: Cell pyroptosis was measured by Cell Counting Kit-8 and flow cytometry analyses. Western blot analysis was used to check proteins expression. Results: The cell viability was significantly decreased by lobaplatin treatment. Compared with the control group, the percentage of pyroptosis (PI and Annexin-V double-positive cells) increased after lobaplatin treatment. In addition, lobaplatin induced caspase-3 activation and GSDME cleavage. z-DEVD, a specific inhibitor of caspase-3, reduced lobaplatin-mediated GSDME cleavage and concurrently inhibited pyroptosis. More importantly, GSDME deficiency obviously reduced lobaplatin-induced pyroptosis. Conclusion: These data demonstrated that caspase-3/GSDME axis contributed to the lobaplatin-mediated pyroptosis in cervical cancer cells. This finding indicates that GSDME-mediated pyroptosis is a new mechanism for lobaplatin to kill tumor cells and suggest that caspase-3/GSDME pathway offer new insights into cancer chemotherapy.


2016 ◽  
Vol 12 (3) ◽  
pp. 2184-2188 ◽  
Author(s):  
Huan Liu ◽  
Haijuan Wang ◽  
Chunxiao Li ◽  
Tingting Zhang ◽  
Xiting Meng ◽  
...  

2020 ◽  
Vol 56 (65) ◽  
pp. 9332-9335
Author(s):  
Sandra Estalayo-Adrián ◽  
Salvador Blasco ◽  
Sandra A. Bright ◽  
Gavin J. McManus ◽  
Guillermo Orellana ◽  
...  

Two new water-soluble amphiphilic Ru(ii) polypyridyl complexes were synthesised and their photophysical and photobiological properties evaluated; both complexes showed a rapid cellular uptake and phototoxicity against HeLa cervical cancer cells.


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