The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Cinnamtannin B-1 inhibits cell survival molecules and induces apoptosis in colon cancer
Open accessAbstract
Colon cancer patients receiving chemotherapy continue to be burdened with therapeutic failure and adverse side effects, yielding a need to develop more effective treatments. The present study investigates Cinnamtannin B-1 (CTB-1) as a potential low-toxicity therapeutic alternative for colon cancer. CTB-1-treated DLD-1, COLO 201 and HCT-116 (WT p53 and p53 null) colon cancer cells and CCD 841 CoN normal colon epithelial cells were assessed for changes in survival using MTT assay. The effects of CTB-1 on cell cycle progression and the apoptosis of colon cancer cells were measured using flow cytometry and/or immunofluorescence. The expression profiles of cell survival molecules, particularly apoptotic proteins, in the colon cancer cells were evaluated following CTB-1 treatment via antibody array, then validated by western blot analysis. Additionally, the potential synergy between CTB-1 and 5-fluorouracil (5-FU), a conventional chemotherapeutic agent used in the treatment of colon cancer, against colon cancer cells was assessed using MTT assay and Calcusyn software. The results revealed that CTB-1 significantly decreased the survival of the DLD-1, COLO 201 and HCT-116 cells in a time and/or dose-dependent manner, with minimal cytotoxicity to normal colon cells. CTB-1 treatment was shown to induce cell cycle arrest and apoptosis of DLD-1 and COLO 201 cells. Of note, CTB-1 modulated the expression of several cell survival molecules, which tend to be deregulated in colon cancer, including p53, a key transcription factor involved in apoptosis. The downstream regulation of Bcl-2 and Bak expression, as well as cytochrome c release into the cytosol, was also observed following CTB-1 treatment. Furthermore, CTB-1 was shown to significantly enhance the potency of 5-FU via a synergistic drug interaction. This study reveals for the first time, to the best of our knowledge, the ability of CTB-1 to decrease the survival of colon cancer cells through pro-apoptotic mechanisms and display synergy with conventional chemotherapy, demonstrating the potential therapeutic benefit of CTB-1 in colon cancer.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“PAs have been shown to have multiple therapeutic effects in both malignant and normal tissues, including anti-angiogenesis, pro-apoptosis, and epigenetic changes.”
From The Synergistic Effect of Proanthocyanidin and HDAC Inhibitor Inhibit Breast Cancer Cell Growth and Promote Apoptosis (2023) · cites this paper as [24]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Combining PAs with other drugs can also enhance the effects of the other drugs [23,24].”
From The Synergistic Effect of Proanthocyanidin and HDAC Inhibitor Inhibit Breast Cancer Cell Growth and Promote Apoptosis (2023) · cites this paper as [24]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Fridman, J. S., & Lowe, S. W. (2003) · Oncogene · doi:10.1038/sj.onc.1207116 · Cited by 1,401
Haupt, S., Berger, M., Goldberg, Z., & Haupt, Y. (2003) · Journal of Cell Science · doi:10.1242/jcs.00739 · Cited by 1,136
Flagged first, then by citations
Research works printed but not linked: 62
- Siegel, 2017, Cancer Statistics, 2017, CA Cancer J Clin, 67, 7, 10.3322/caac.21387 · DOI · Paper page
- Howlader, 2016, SEER Cancer Statistics Review, 1975–2013
- Braun, 2011, Balancing the efficacy and toxicity of chemotherapy in colorectal cancer, Ther Adv Med Oncol, 3, 43, 10.1177/1758834010388342 · DOI · Paper page
- Hu, 2012, Adjuvant chemotherapy and risk of gastrointestinal, hematologic, and cardiac toxicities in elderly patients with stage III colon cancer, Am J Clin Oncol, 35, 228, 10.1097/COC.0b013e318210f812 · DOI
- Nadeem, 2014, Cost differential among systemic therapies for colon cancer, Ann Surg Oncol, 21, S83
- Liu, 2011, The efficacy of chemotherapy in patients with high-grade metastatic colon cancer, Hepatogastroenterology, 58, 1495, 10.5754/hge11082 · DOI
- Engstrom, 2009, NCCN Clinical Practice Guidelines in Oncology: Colon cancer, J Natl Compr Canc Netw, 7, 778, 10.6004/jnccn.2009.0056 · DOI
- Patel, 2008, Curcumin enhances the effects of 5-fluorouracil and oxaliplatin in mediating growth inhibition of colon cancer cells by modulating EGFR and IGF-1R, Int J Cancer, 122, 267, 10.1002/ijc.23097 · DOI
- Patel, 2010, Curcumin targets FOLFOX-surviving colon cancer cells via inhibition of EGFRs and IGF-1R, Anticancer Res, 30, 319
- Chen, 2014, Effectiveness of a novel herbal agent MB-6 as a potential adjunct to 5-fluoracil-based chemotherapy in colorectal cancer, Nutr Res, 34, 585, 10.1016/j.nutres.2014.06.010 · DOI
- Amin, 2009, Perspectives for cancer prevention with natural compounds, J Clin Oncol, 27, 2712, 10.1200/JCO.2008.20.6235 · DOI
- Plumb, 1998, Antioxidant properties of catechins and proanthocyanidins: Effect of polymerisation, galloylation and glycosylation, Free Radic Res, 29, 351, 10.1080/10715769800300391 · DOI
- Santos-Buelga, 2000, Proanthocyanidins and tannin-like compounds - nature, occurrence, dietary intake and effects on nutrition and health, J Sci Food Agric, 80, 1094, 10.1002/(SICI)1097-0010(20000515)80:7<1094::AID-JSFA569>3.0.CO;2-1 · DOI
- Prasad, 2012, Grape proanthocyanidin inhibit pancreatic cancer cell growth in vitro and in vivo through induction of apoptosis and by targeting the PI3K/Akt pathway, PLoS One, 7, e43064, 10.1371/journal.pone.0043064 · DOI
- Sharma, 2010, Proanthocyanidins inhibit in vitro and in vivo growth of human non-small cell lung cancer cells by inhibiting the prostaglandin E(2) and prostaglandin E(2) receptors, Mol Cancer Ther, 9, 569, 10.1158/1535-7163.MCT-09-0638 · DOI
- Singh, 2011, Grape proanthocyanidins induce apoptosis by loss of mitochondrial membrane potential of human non-small cell lung cancer cells in vitro and in vivo, PLoS One, 6, e27444, 10.1371/journal.pone.0027444 · DOI
- Nomoto, 2004, Chemoprevention of colorectal cancer by grape seed proanthocyanidin is accompanied by a decrease in proliferation and increase in apoptosis, Nutr Cancer, 49, 81, 10.1207/s15327914nc4901_11 · DOI
- Chen, 2014, Grape seed proanthocyanidins (GSPs) inhibit the growth of cervical cancer by inducing apoptosis mediated by the mitochondrial pathway, PLoS One, 9, e107045, 10.1371/journal.pone.0107045 · DOI
- Vaid, 2011, Grape seed proanthocyanidins inhibit melanoma cell invasiveness by reduction of PGE2 synthesis and reversal of epithelial-to-mesenchymal transition, PLoS One, 6, e21539, 10.1371/journal.pone.0021539 · DOI
- Engelbrecht, 2007, Proanthocyanidin from grape seeds inactivates the PI3-kinase/PKB pathway and induces apoptosis in a colon cancer cell line, Cancer Lett, 258, 144, 10.1016/j.canlet.2007.08.020 · DOI
- Nandakumar, 2008, Multi-targeted prevention and therapy of cancer by proanthocyanidins, Cancer Lett, 269, 378, 10.1016/j.canlet.2008.03.049 · DOI · Paper page
- Ting-Ting, 2012, Inhibitive effect of proanthocyanidins on cyclooxygenase-2 expression in A549 cells induced by cytokine interleukin-1 beta, J Shanghai Jiaotong Univ, 17, 500, 10.1007/s12204-012-1312-y · DOI
- Jayaprakasha, 2006, Phenolic constituents in the fruits of Cinnamomum zeylanicum and their antioxidant activity, J Agric Food Chem, 54, 1672, 10.1021/jf052736r · DOI
- Dall'Acqua, 2009, Phytochemical composition and antioxidant activity of Laurus nobilis L, leaf infusion J Med Food, 12, 869, 10.1089/jmf.2008.0119 · DOI
- Taher, 2006, Majid F adibah abdul and Sarmidi MRS: A proanthocyanidin from cinnamomum zeylanicum stimulates phosphorylation of insulin receptor in 3t3-l1 adipocytes, J Teknol, 44, 53
- Bouaziz, 2007, Cinnamtannin B-1 from bay wood reduces abnormal intracellular Ca2+ homeostasis and platelet hyperaggregability in type 2 diabetes mellitus patients, Arch Biochem Biophys, 457, 235, 10.1016/j.abb.2006.10.020 · DOI
- Ben Amor, 2007, Characterization of the intracellular mechanisms involved in the antiaggregant properties of cinnamtannin B-1 from bay wood in human platelets, J Med Chem, 50, 3937, 10.1021/jm070508d · DOI
- Bouaziz, 2007, Cinnamtannin B-1 from bay wood exhibits antiapoptotic effects in human platelets, Apoptosis, 12, 489, 10.1007/s10495-006-0014-z · DOI
- Wen, 2015, Identification of phenolics in litchi and evaluation of anticancer cell proliferation activity and intracellular antioxidant activity, Free Radic Biol Med, 84, 171, 10.1016/j.freeradbiomed.2015.03.023 · DOI
- Kashiwada, 1992, Antitumor agents, 129. Tannins and related compounds as selective cytotoxic agents, J Nat Prod, 55, 1033, 10.1021/np50086a002 · DOI
- Chou, 1983, Analysis of combined drug effects: A new look at a very old problem, Trends Pharmacol Sci, 4, 450, 10.1016/0165-6147(83)90490-X · DOI
- Chou, 1984, Quantitative analysis of dose-effect relationships: The combined effects of multiple drugs or enzyme inhibitors, Adv Enzyme Regul, 22, 27, 10.1016/0065-2571(84)90007-4 · DOI · Paper page
- Chou, 2010, Drug combination studies and their synergy quantification using the Chou-Talalay method, Cancer Res, 70, 440, 10.1158/0008-5472.CAN-09-1947 · DOI · Paper page
- Kelly, 2007, Chemotherapy in metastatic colorectal cancer, Surg Oncol, 16, 65, 10.1016/j.suronc.2007.04.006 · DOI
- Chibaudel, 2012, Therapeutic strategy in unresectable metastatic colorectal cancer, Ther Adv Med Oncol, 4, 75, 10.1177/1758834011431592 · DOI
- Goodwin, 2009, Overview of systemic therapy for colorectal cancer, Clin Colon Rectal Surg, 22, 251, 10.1055/s-0029-1242465 · DOI
- Hanahan, 2011, Hallmarks of cancer: The next generation, Cell, 144, 646, 10.1016/j.cell.2011.02.013 · DOI · Paper page
- Abraha, 2016, Apoptotic pathways as a therapeutic target for colorectal cancer treatment, World J Gastrointest Oncol, 8, 583, 10.4251/wjgo.v8.i8.583 · DOI
- Lane, 1992, Cancer. p53, guardian of the genome, Nature, 358, 15, 10.1038/358015a0 · DOI · Paper page
- Higashimoto, 2000, Human p53 is phosphorylated on serines 6 and 9 in response to DNA damage-inducing agents, J Biol Chem, 275, 23199, 10.1074/jbc.M002674200 · DOI
- Kaeser, 2004, Regulation of p53 stability and function in HCT116 colon cancer cells, J Biol Chem, 279, 7598, 10.1074/jbc.M311732200 · DOI
- Schuler, 2000, p53 induces apoptosis by caspase activation through mitochondrial cytochrome c release, J Biol Chem, 275, 7337, 10.1074/jbc.275.10.7337 · DOI
- Soussi, 2006, Locus-specific mutation databases: Pitfalls and good practice based on the p53 experience, Nat Rev Cancer, 6, 83, 10.1038/nrc1783 · DOI
- Siegel, 2014, Cancer Stat, 2014, 9
- Hemann, 2006, The p53-Bcl-2 connection, Cell Death Differ, 13, 1256, 10.1038/sj.cdd.4401962 · DOI
- Al-Suhaibani, 2015, Antiproliferation and antiactivity of proanthocyanidins against colorectal cancer cells (Caco-2) line through mitochondrial pathway, Int J Adv Sci Tech Res, 4, 152
- Roy, 2005, Grape seed proanthocyanidins induce apoptosis through p53, Bax, and caspase 3 pathways, Neoplasia, 7, 24, 10.1593/neo.04412 · DOI
- Liu, 2006, Analysis of P53 mutations and their expression in 56 colorectal cancer cell lines, Proc Natl Acad Sci USA, 103, 976, 10.1073/pnas.0510146103 · DOI · Paper page
- Yoo, 2007, Targeting thioredoxin reductase 1 reduction in cancer cells inhibits self-sufficient growth and DNA replication, PLoS One, 2, e1112, 10.1371/journal.pone.0001112 · DOI
- Sun, 2009, To C or not to C: Direct and indirect redox regulation of Src protein tyrosine kinase, Cell Cycle, 8, 2353, 10.4161/cc.8.15.9225 · DOI
- Vaughn, 2008, Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrom c, Nat Cell Biol, 10, 1477, 10.1038/ncb1807 · DOI
- Salvioli, 2003, Apoptosis-resistant phenotype in HL-60-derived cells HCW-2 is related to changes in expression of stress-induced proteins that impact on redox status and mitochondrial metabolism, Cell Death Differ, 10, 163, 10.1038/sj.cdd.4401124 · DOI
- Mileo, 2016, Polyphenols as modulator of oxidative stress in cancer disease: New therapeutic strategies, Oxid Med Cell Longev, 2016, 6475624, 10.1155/2016/6475624 · DOI
- Cos, 2004, Proanthocyanidins in health care: Current and new trends, Curr Med Chem, 11, 1345, 10.2174/0929867043365288 · DOI
- Lee, 2012, Wogonin induces apoptosis by activating the AMPK and p53 signaling pathways in human glioblastoma cells, Cell Signal, 24, 2216, 10.1016/j.cellsig.2012.07.019 · DOI
- Sharif, 2010, Red wine polyphenols cause growth inhibition and apoptosis in acute lymphoblastic leukaemia cells by inducing a redox-sensitive up-regulation of p73 and down-regulation of UHRF1, Eur J Cancer, 46, 983, 10.1016/j.ejca.2009.12.029 · DOI
- Shankar, 2007, Involvement of Bcl-2 family members, phosphatidylinositol 3'-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer, Int J Oncol, 30, 905
- Ye, 2004, The isoflavonoids genistein and quercetin activate different stress signaling pathways as shown by analysis of site-specific phosphorylation of ATM, p53 and histone H2AX, DNA Repair (Amst), 3, 235, 10.1016/j.dnarep.2003.10.014 · DOI
- Su, 2006, Curcumin-induced apoptosis of human colon cancer colo 205 cells through the production of ROS, Ca2+ and the activation of caspase-3, Anticancer Res, 26, 4379
- Méplan, 2000, Redox signalling and transition metals in the control of the p53 pathway, Biochem Pharmacol, 59, 25, 10.1016/S0006-2952(99)00297-X · DOI
- Maillet, 2012, Redox regulation of p53, redox effectors regulated by p53: A subtle balance, Antioxid Redox Signal, 16, 1285, 10.1089/ars.2011.4434 · DOI
- Liu, 2008, ROS and p53: A versatile partnership, Free Radic Biol Med, 44, 1529, 10.1016/j.freeradbiomed.2008.01.011 · DOI
Cited by
Sorted by citations
Wang, T. K., Xu, S., Fan, Y., Wu, J., Wang, Z., Chen, Y., & Zhang, Y. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241310476 · Cited by 18
“Combining PAs with other drugs can also enhance the effects of the other drugs [23,24].”
Background
Metadata
- Authors
- Carriere, P., Kapur, N., Mir, H., Ward, A., & Singh, S.
- Affiliations
- Morehouse School of Medicine (US)
- Corresponding author
- Singh, Shailesh
- Venue
- International Journal of Oncology
- Publisher
- Spandidos Publications
- Published
- 2018-07-19
- Volume
- 53
- Issue
- 4
- Pages
- 1442-1454
- ISSN
- 1019-6439 (ISSN-L)
- 1791-2423
- PMC
- PMC6086629
- OpenAlex
- W2884690170
- Cited by
- 18
- References
- 2
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 4 · 2020: 4 · 2019: 3
- FWCI
- 1.08
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- International Journal of Oncology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- University of Alabama at Birmingham
- University of Alabama
- Morehouse School of Medicine
- National Institutes of Health (CA118638)
- National Cancer Institute (CA179701, SC1CA180212, CA169716, CA118638, R21CA169716, U01CA179701, CA180212)
- Topics
- Physical Sciences › Chemistry › Organic Chemistry › Tannin, Tannase and Anticancer Activities
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Physical Sciences › Chemistry › Organic Chemistry › Natural product bioactivities and synthesis
- Keywords
- colon cancer, apoptosis, p53, Bcl-2, Bak, cytochrome c release, cell cycle arrest, 5-fluorouracil, drug synergy, anticancer natural products, DLD-1 cells, HCT116 cells
- MeSH terms
- Antineoplastic Combined Chemotherapy Protocols, Cell Survival, Colonic Neoplasms, Dose-Response Relationship, Drug, Drug Synergism, Fluorouracil, Humans, Treatment Outcome, Apoptosis, Gene Expression Profiling, Proanthocyanidins, Cell Line, Tumor, Apoptosis Regulatory Proteins, Cell Cycle Checkpoints
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review