ArticleCancer management and research2019
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Computational and Cytotoxicity Evaluation of Phyllanthus Urinaria-Derived Compounds as Potential Anti-Cervical Cancer Agents via HPV-16 E6 Oncoprotein Inhibition.International journal of molecular sciences · 2026Article
- Integrative approach to decipher pharmacological mechanism of Cinnamomum zeylanicum essential oil in prostate cancer.Medical oncology (Northwood, London, England) · 2025Article
- Elucidating the anti-cancer potential ofHeliyon · 2024Article
- Review
- A Comprehensive Review on Pharmacologically Active Phyto-Constituents fromMolecules (Basel, Switzerland) · 2023Review
- Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage.Antioxidants (Basel, Switzerland) · 2023Article
- Anti-proliferative Activity ofCombinatorial chemistry & high throughput screening · 2023Article
- Article
- AZD4547 targets the FGFR/Akt/SOX2 axis to overcome paclitaxel resistance in head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- EphA2 promotes tumorigenicity of cervical cancer by up-regulating CDK6.Journal of cellular and molecular medicine · 2021Article
- Uncharted Source of Medicinal Products: The Case of theMedicines (Basel, Switzerland) · 2020Review
- Article
- BRD4 inhibitor nitroxoline enhances the sensitivity of multiple myeloma cells to bortezomibTherapeutic advances in hematology · 2020Article
- Coronarin D Induces Apoptotic Cell Death and Cell Cycle Arrest in Human Glioblastoma Cell Line.Molecules (Basel, Switzerland) · 2019Article
- IL-2 Induces Transient Arrest in the G1 Phase to Protect Cervical Cancer Cells from Entering Apoptosis.Journal of oncology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMATERIALS AND
methodsThe cytotoxicity of HCEE was evaluated by MTT and clonogenic survival assay. Annexin V/propidium iodide (PI), Hoechst 33342 staining, and TUNEL assay were performed to detect apoptosis. Cell cycle analysis was performed using PI staining. JC-1 and 2',7'-dichlorodihydrofluorescein diacetate assay were used to check the levels of MMP and ROS, respectively. Western blot analysis was carried out to measure the expression levels of proteins. Migration and invasion activity were assessed by wound healing and Transwell membrane assay, respectively.
resultsAntiproliferative effect of HCEE was investigated in various cancerous and normal cell lines. Among these, HCEE significantly inhibited the survival of HeLa cells without affecting the viability of normal human umbilical vein endothelial cells. Annexin V/PI, Hoechst staining, and TUNEL assay showed HCEE induced apoptosis in HeLa cells in a dose-dependent manner. HCEE promoted cell cycle arrest at G1 phase in HeLa cells by upregulating the levels of p53 and p21 and downregulating the levels of cyclin D1, CDK-4, and CDK-6. Moreover, HCEE treatment upregulated the expression of Bax and downregulated the expression of Bcl-2. Additionally, HCEE activated the caspase cascade by increasing the activities of caspase-9, caspase-8, and caspase-3. The expression levels of Fas ligand and Fas were also upregulated. Further, HCEE inhibited the migratory potential of HeLa cells by downregulating MMP-2 and MMP-9 expression levels.
conclusionOur results indicate
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.