scholarly journals Heavy-Ion Carbon Radiation Regulates Long Non-Coding RNAs in Cervical Cancer HeLa Cells

2019 ◽  
Vol 10 (21) ◽  
pp. 5022-5030
Author(s):  
Zhi Yang ◽  
Qingying Gu ◽  
Ying Wang ◽  
Bo Liu ◽  
Guangming Zhou ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Heavy Ion ◽  
Non Coding Rnas

scholarly journals Inhibition of Wnt-β-Catenin Signaling by ICRT14 Drug Depends of Post-Transcriptional Regulation by HOTAIR in Human Cervical Cancer HeLa Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Samuel Trujano-Camacho ◽  
David Cantú-de León ◽  
Izamary Delgado-Waldo ◽  
Jossimar Coronel-Hernández ◽  
Oliver Millan-Catalan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Transcriptional Activity ◽  
Hpv Infection ◽  
Target Therapies ◽  
Non Coding Rnas ◽  
Inhibitory Drug ◽  
Preclinical And Clinical Studies ◽  
Post Transcriptional Regulation

BackgroundIn Cervical cancer (CC), in addition to HPV infection, the most relevant alteration during CC initiation and progression is the aberrant activation of Wnt/β-catenin pathway. Several inhibitory drugs of this pathway are undergoing preclinical and clinical studies. Long non-coding RNAs (lncRNAs) are associated with resistance to treatments. In this regard, understanding the efficiency of drugs that block the Wnt/β-catenin pathway in CC is of relevance to eventually propose successful target therapies in patients with this disease.MethodsWe analyzed the levels of expression of 249 components of the Wnt/β-catenin pathway in a group of 109 CC patients. Three drugs that blocking specific elements of Wnt/β-catenin pathway (C59, NSC668036 and ICRT14) by TOP FLASH assays and qRT-PCR were tested in vitro in CC cells.Results137 genes of the Wnt/β-catenin pathway were up-regulated and 112 down-regulated in CC patient’s samples, demonstrating that this pathway is dysregulated. C59 was an efficient drug to inhibit Wnt/β-catenin pathway in CC cells. NSC668036, was not able to inhibit the transcriptional activity of the Wnt/β-catenin pathway. Strikingly, ICRT14 was neither able to inhibit this pathway in HeLa cells, due to HOTAIR interaction with β-catenin, maintaining the Wnt/β-catenin pathway activated.ConclusionsThese results demonstrate a mechanism by which HOTAIR evades the effect of ICRT14, a Wnt/β-catenin pathway inhibitory drug, in HeLa cell line. The emergence of these mechanisms reveals new scenarios in the design of target therapies used in cancer.

scholarly journals SOX2 Regulates lncRNA CCAT1/MicroRNA-185-3p/FOXP3 Axis to Affect the Proliferation and Self-Renewal of Cervical Cancer Stem Cells

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Li Zhang ◽  
Chunjie Guo ◽  
Tiefeng Ji ◽  
Xin Chen
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Hela Cells ◽  
Self Renewal ◽  
Inhibition Of Proliferation ◽  
Forkhead Box ◽  
Gynecology And Obstetrics ◽  
Non Coding Rnas ◽  
The Relationship

AbstractIt has been presented the role of long non-coding RNAs (lncRNAs) in cervical cancer (CC). We aim to discuss the effect of sex-determining region Y-box 2 (SOX2)/lncRNA colon cancer-associated transcript-1 (CCAT1)/microRNA-185-3p (miR-185-3p)/forkhead box protein 3 (FOXP3) on the proliferation and self-renewal ability of CC stem cells. MiR-185-3p, SOX2, CCAT1 and FOXP3 expressions were tested in CC tissues and cells. The relationship between SOX2/CCAT1 expression and clinicopathological features in CC patients was verified. Loss- and gain-of-function investigations were conducted in CD44+HeLa cells to discuss biological functions and self-renewal capacity. Finally, the relationships among SOX2, CCAT1, FOXP3 and miR-185-3p were verified. miR-185-3p expression was decreased, while SOX2, CCAT1 and FOXP3 expressions were increased in CC tissues and cells. SOX2 and CCAT1 expressions were linked to tumor size, lymph node metastasis and international federation of gynecology and obstetrics stage of CC. Down-regulating SOX2 or CCAT1 and up-regulating miR-185-3p resulted in inhibition of proliferation, invasion, migration and cell sphere number as well as apoptosis acceleration of CD44+HeLa cells. SOX2 could bind to CCAT1 which affected miR-185-3p expression, and FOXP3 was targeted by miR-185-3p.

Effects of Papaya Leaf Extract (Carica papaya L.) on Cellular Proliferation and Apoptosis in Cervical Cancer Mice Model

2019 ◽  
Vol 17 (5) ◽  
pp. 265-275
Author(s):  
Y. Peristiowati ◽  
Y. Puspitasari ◽  
Indasah
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Hela Cells ◽  
Leaf Extract ◽  
Caspase 3 ◽  
Methanol Extract ◽  
Negative Control ◽  
Proliferation Index ◽  
Control Group ◽  
P53 Expression

This study is aimed at analyzing the anticancer properties of papaya leaf extract, specifically the inhibition of cell proliferation and apoptotic induction through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and p53 pathways. Twenty-five mice (Mus musculus), aged 2 months and weighing 20–30 g, was injected with 0.5 mg dexamethasone for 7 days. The mice were then injected intracutaneously with 1 ml of HeLa cells (8 × 106 HeLa cells/microliter). The mice were divided into five groups (5 each): negative control (P1) (5% CMC-Na, sodium carboxymethyl cellulose), treatment II (225 mg/kg BW (body weight) papaya leaves methanol extract), treatment III (450 mg/kg BW), treatment IV (750 mg/kg BW), and treatment PV (2 mg alcohol anticancer drug). Papaya leaf extract treatments were applied for 2 weeks. Then, the tumor tissue was isolated for hematoxylin and eosin staining. Immunohistochemical imaging was used to detect Ki-67, caspase-3, NF-κB, and p53 expression. Further analysis was undertaken using the ImmunoRatio software program. The results indicated that administration of papaya leaf methanol extract significantly increased the expression of NF-κB and p53 at a dose of 450 mg/kg BW. Our results also showed that the mice treated with 450 mg of papaya leaf extract per kg of BW (P3) had the largest increase of caspase-3 expression compared to the negative control group. Papaya leaf ethanol extract decreased the cancer cell proliferation index and increased apoptosis of cancer cells in animal models of cervical cancer; it may also work to increase NF-kB expression and expression of the p53 gene.

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

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.

scholarly journals Secondary Structural Model of MALAT1 Becomes Unstructured in Chronic Myeloid Leukemia and Undergoes Structural Rearrangement in Cervical Cancer

2021 ◽  
Vol 7 (1) ◽  
pp. 6
Author(s):  
Matthew C. Wang ◽  
Phillip J. McCown ◽  
Grace E. Schiefelbein ◽  
Jessica A. Brown
Keyword(s):  
Cervical Cancer ◽  
Chronic Myeloid Leukemia ◽  
Hela Cells ◽  
Binding Sites ◽  
Myeloid Leukemia ◽  
Structural Changes ◽  
Structural Model ◽  
Dimethyl Sulfate ◽  
K562 Cells ◽  
Cancer Types

Long noncoding RNAs (lncRNAs) influence cellular function through binding events that often depend on the lncRNA secondary structure. One such lncRNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is upregulated in many cancer types and has a myriad of protein- and miRNA-binding sites. Recently, a secondary structural model of MALAT1 in noncancerous cells was proposed to form 194 hairpins and 13 pseudoknots. That study postulated that, in cancer cells, the MALAT1 structure likely varies, thereby influencing cancer progression. This work analyzes how that structural model is expected to change in K562 cells, which originated from a patient with chronic myeloid leukemia (CML), and in HeLa cells, which originated from a patient with cervical cancer. Dimethyl sulfate-sequencing (DMS-Seq) data from K562 cells and psoralen analysis of RNA interactions and structure (PARIS) data from HeLa cells were compared to the working structural model of MALAT1 in noncancerous cells to identify sites that likely undergo structural alterations. MALAT1 in K562 cells is predicted to become more unstructured, with almost 60% of examined hairpins in noncancerous cells losing at least half of their base pairings. Conversely, MALAT1 in HeLa cells is predicted to largely maintain its structure, undergoing 18 novel structural rearrangements. Moreover, 50 validated miRNA-binding sites are affected by putative secondary structural changes in both cancer types, such as miR-217 in K562 cells and miR-20a in HeLa cells. Structural changes unique to K562 cells and HeLa cells provide new mechanistic leads into how the structure of MALAT1 may mediate cancer in a cell-type specific manner.

Identification of Chemo and Radio-resistant Sub-population of Stem Cells in Human Cervical Cancer HeLa Cells

2021 ◽  
pp. 1-27
Author(s):  
Nabil Mohie Abdel-Hamid ◽  
Moustafa Fathy ◽  
Chika Koike ◽  
Toshiko Yoshida ◽  
Motonori Okabe ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Hela Cells ◽  
Human Cervical Cancer

scholarly journals Apoptotic effect of novel pyrazolone-based derivative [Cu(PMPP-SAL)(EtOH)] on HeLa cells and its mechanism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Delizhaer Reheman ◽  
Jing Zhao ◽  
Shan Guan ◽  
Guan-Cheng Xu ◽  
Yi-Jie Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Hela Cells ◽  
Copper Complexes ◽  
Antibacterial Properties ◽  
Inhibitory Effect ◽  
Parp Cleavage ◽  
Potential Candidate ◽  
Tnf Α

Abstract Pyrazolone complexes have strong anti-tumor and antibacterial properties, but the anti-tumor mechanism of pyrazolone-based copper complexes has not been fully understood. In this study, the possible mechanism and the inhibitory effect of a novel pyrazolone-based derivative compound [Cu(PMPP-SAL)(EtOH)] on human cervical cancer cells (HeLa cells) was investigated. [Cu(PMPP-SAL)(EtOH)] effectively inhibited proliferation of HeLa cells in vitro with an IC50 value of 2.082 after treatment for 72 h. Cell cycle analysis showed apoptosis was induced by blocking the cell cycle in the S phase. [Cu(PMPP-SAL)(EtOH)] promoted the loss of mitochondrial membrane potential, release of cytochrome c, PARP cleavage, and activation of caspase-3/9 in HeLa cells. Additionally, [Cu(PMPP-SAL)(EtOH)] inhibited the PI3K/AKT pathway and activated the P38/MAPK, and JNK/MAPK pathways. [Cu(PMPP-SAL)(EtOH)] also inhibited the phosphorylation of Iκ-Bα in the NF-κB pathway activated by TNF-α, thus restricting the proliferation of HeLa cells which were activated by TNF-α. In conclusion, [Cu(PMPP-SAL)(EtOH)] inhibited the growth of HeLa cells and induced apoptosis possibly via the caspase-dependent mitochondria-mediated pathway. These results suggest that [Cu(PMPP-SAL)(EtOH)] can be a potential candidate for the treatment of cervical cancer.

scholarly journals The Inhibitory Effect of a Novel Polypeptide Fraction fromArca subcrenataon Cancer-Related Inflammation in Human Cervical Cancer HeLa Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Yu Wu ◽  
Xianjing Hu ◽  
Liyan Song ◽  
Jianhua Zhu ◽  
Rongmin Yu
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Molecular Mechanisms ◽  
Tumor Development ◽  
Basic Research ◽  
Inhibitory Effect ◽  
Fishery Resource ◽  
Proinflammatory Mediators ◽  
Raw264.7 Macrophage ◽  
Human Cervical Cancer

Inflammation is known to be closely associated with the development of cancer. The study was launched in human cervical cancer HeLa cells to investigate the antitumor and anti-inflammatory effects of P2, a marine polypeptide fraction from an important fishery resourceArca subcrenata. The basic research showed that P2 could suppress the production of nitric oxide in LPS-induced RAW264.7 macrophage cells as well as the secretion of inflammatory cytokines IL-6 and TNF-αin human cervical cancer HeLa cells. For the molecular mechanisms, P2 was shown to downregulate the gene expression of proinflammatory cytokines IL-6 and IL-8 and to inhibit the COX-2 and iNOS-related pathways in HeLa cells. In consequence, P2 might inhibit tumor development by blocking the interaction between tumor microenvironment and proinflammatory mediators. All findings indicate that P2 possesses the potential to be developed as a novel agent for cancer therapy.

Apigetrin Promotes Cell Autophagy by Activating the Endoplasmic Reticulum Stress in Human Cervical Cancer Hela Cells

2021 ◽  
Vol 20 (1) ◽  
pp. 56-63
Author(s):  
Li Jiang ◽  
Zhi-Cheng Yao ◽  
Miao-Miao Liu ◽  
Run-Hui Ma ◽  
Kiran Thakur
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Hela Cells ◽  
Fruits And Vegetables ◽  
Radical Scavenging ◽  
Anticancer Activities ◽  
Treatment Results ◽  
Metastasis Rate ◽  
The Relationship

Cervical cancer has always been the top malignant cancer among female cancers in the world. Due to its recurrence, metastasis rate, and drug resistance, the treatment results of cervical cancer have been unsatisfactory. Apigetrin is present in a variety of fruits and vegetables and has been reported to have antioxidant, free radical scavenging, anti-inflammatory, and anticancer activities. Therefore, this study focuses on the effect of apigetrin on the autophagy of cervical cancer HeLa cells based on the previous research. The results showed that apigetrin can enhance the autophagy fluorescence of light chain 3B (LC3B), and further combined with quantitative real-time PCR (qPCR) and Western blotting found that the expression of autophagy-related genes and proteins p-mTOR, Beclin1, and LC3B increased, while the expression of AMPK, ULK1, and p62 decreased. In addition, apigetrin also promoted the release of Ca2+, the PERK/eIF2α/ATF4/chop, and IRE1α pathways activate endoplasmic reticulum (ER) stress. The addition of 4PBA proved that ER stress promoted autophagy in HeLa cells. Finally, the addition of the 3-MA indicates the relationship between autophagy and apoptosis in HeLa cells. Our results indicate that apigetrin has a certain anticancer potential and can be used as a drug adjuvant and food additive for the prevention and treatment of cervical cancer.

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