ArticleCancer science2019
All-trans retinoic acid reverses epithelial-mesenchymal transition in paclitaxel-resistant cells by inhibiting nuclear factor kappa B and upregulating gap junctions.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- FAM107A inhibits Invasion and migration of colorectal cancer by affecting EMT via the AKT pathway.Histology and histopathology · 2026Article
- Multicomponent Ganoderma lucidum spore-based solid self-nanoemulsifying system of paclitaxel for improved lymphatic absorption and immune synergistic antitumor strategy.Journal of nanobiotechnology · 2026Article
- Pleiotropic effects of all-trans retinoic acid in attenuating the hallmarks of colorectal cancer- challenges and scope of differentiation therapy.Cancer gene therapy · 2026Review
- Combination of cellular retinoic acid-binding protein 2 overexpression and all-trans retinoic acid synergistically inhibits oesophageal squamous cell carcinoma progression.Discover oncology · 2025Article
- Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024Review
- Interplay between paclitaxel, gap junctions, and kinases: unraveling mechanisms of action and resistance in cancer therapy.Molecular biology reports · 2024Review
- Cellular and micro-environmental responses influencing the antitumor activity of all-trans retinoic acid in breast cancer.Cell communication and signaling : CCS · 2024Review
- Cell Death, by Any Other Name….Cells · 2024Review
- Vitamin A, D, E, and K as Matrix Metalloproteinase-2/9 Regulators That Affect Expression and Enzymatic Activity.International journal of molecular sciences · 2023Review
- Caspase-9-mediated cleavage of vimentin attenuates the aggressiveness of leukemic NB4 cells.Molecular and cellular biochemistry · 2023Article
- Platycodin D represses β-catenin to suppress metastasis of cetuximab-treated KRAS wild-type colorectal cancer cells.Clinical & experimental metastasis · 2023Article
- 13‑International journal of molecular medicine · 2023Article
- Chemotherapeutic properties and side-effects associated with the clinical practice of terpene alkaloids: paclitaxel, docetaxel, and cabazitaxel.Frontiers in pharmacology · 2023Review
- Epithelial-mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities.MedComm · 2022Review
- Therapeutic Role of Carotenoids in Blood Cancer: Mechanistic Insights and Therapeutic Potential.Nutrients · 2022Review
- A modified parachute assay for assessment of gap junction intercellular communication in placental trophoblast cells.Toxicology mechanisms and methods · 2021Article
- Eubacterium rectale contributes to colorectal cancer initiation via promoting colitis.Gut pathogens · 2021Article
- Carotenoids in Cancer Metastasis-Status Quo and Outlook.Biomolecules · 2020Review
- Article
- Connexins-Therapeutic Targets in Cancers.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Paclitaxel is a widely used chemotherapy drug, but development of resistance leads to treatment failure. Tumor cells that are treated with a sublethal dose of paclitaxel for a long period of time show the epithelial-mesenchymal transition (EMT) phenotype, which leads to metastasis and resistance. All-trans retinoic acid (ATRA) is always used in combination with paclitaxel and can reverse EMT in many types of cancer cells. The ability of ATRA to reverse EMT in chemoresistant cells is still unknown. In the present study, the ability of ATRA to reverse EMT in paclitaxel-resistant cells was investigated. Three colorectal cancer cell lines, HCT116, LoVo and CT26, were treated with sublethal doses of paclitaxel to create resistant cell lines. Western blotting, immunocytochemistry, and "parachute" dye-coupling assays showed that ATRA reverses EMT, inhibits nuclear factor kappa B (NF-κΒ), and upregulates gap junctions in paclitaxel-resistant cells. Scratch wound-healing and Transwell assays showed that ATRA decreases the migration and invasion abilities of paclitaxel-resistant cells. In addition, the CT26 cell line was used in the Balb/c pulmonary metastasis model to show that ATRA reduces metastasis of paclitaxel-resistant cells in vivo. Given these data, ATRA may reverse EMT by inhibiting NF-κΒ and upregulating gap junctions in paclitaxel-resistant cells.
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.