Chemistry, Biology and Cancer: The Bond

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Kausar et al 61 showed that the thiols act as the intermediate between Cucurbitacin B and its toxicity in lung cancer cells.

Understanding and controlling molecules related to cancer metastasis through chemical biology

Lung cancer when treated with cucurbitacin B inhibited phosphorylation of STAT3 to cause growth arrest and apoptosis in dose- and time-dependent manner They reported that the altered histone modifications at the respective promoter sites caused upregulation of p16 INK4A and p21 WAF1 and downregulation of hTERT to cause replicative senescence, growth arrest and apoptosis. The results were validated using carcinogen NNK-induced lung tumorigenesis in mice, advocating epigenetic modulation to be a significant anticancer mechanism of cucurbitacin B.

The treatment delayed cell migration, alleviated invasion potential and caused dose- and time-dependent apoptosis. It also showed potent anti-angiogenic effects. All the results were validated using NNK-induced lung tumorigenesis in mice. Intraperitoneal injections of cucurbitacin B at 0. In malignant melanoma, cucurbitacin B inhibited cell proliferation as well as their migratory potential There was significant depletion and aggregation of G-actin protein from the cellular cytoskeleton, reversed using NAC.

NAC is an N-acetyl derivative of L -cysteine and an established potent antioxidant. Cofilin is an actin-depolymerization factor. It is regulated by phosphatidylinositol phosphate, pH variations, redox balance and competition with tropomyosins 68 , activated by dephosphorylation at its serine residue 3 by chronotropin or slingshot phosphatases, and inactivated by phosphorylation via LIM or TES kinases Rho-associated kinases indirectly modulate the stress fibers and focal adhesions Cofilin and actin form rods and are implicated in the pathogenesis of neurogenerative disorders Cucurbitacin B dramatically activated cofilin via thiol oxidation, which formed rod-like structures co-localizing with the actin tandem rods in melanoma cells Cucurbitacin B induced slingshot homolog-1 dependent hyper activation of cofilin and formation of cofilin-actin rods downstream of actin aggregation.

VASP, an F-actin barbed end binding protein facilitates actin filament elongation through interaction with G-actin, profilin and other actin regulatory factors It directly controls the assembly of the actin-filament mesh, transforms the morphology and behavior of membrane protrusion structures and also contributes to cell migration and adhesion. These clumps co-localized with amorphous actin aggregates, prior to the formation of highly ordered cofilin-actin rods in melanoma cells.

Cucurbitacin B inhibited growth of human glioblastoma multiforme cells by intense disturbance in its internal cytoskeleton Within 15—30 min of treatment, it caused loss of pseudopodia, multi-nucleation and skirting up of cells associated with disruption of actin and microtubules, but was followed by the activation of cell survival pathways. SP blocked the effects of cucurbitacin B. Laminins and fibronectin are extracellularly present high molecular weight cell adhesion proteins, and constitute major component of basal lamina contributing to cell adherence, dissemination and differentiation.

Their upregulation is commonly found in EMT. Authors found significant downregulation of Laminin-1 and fibronectin in human glioblastoma cells. Further introspection in microvasculature endothelial cells demonstrated potent anti-angiogenic activity. Cucurbitacin B also showed remarkable anticancer effects in human neuroblastoma cancer cell lines This was accompanied with the downregulation of proteins CDK1 and cyclin B1 essential for cell cycle progression.

Shang et al 78 reported that PTEN activation is crucial and adds positively to the anti-proliferative effects of cucurbitacin B. Apart from proliferation inhibition, cell cycle restraining and apoptotic trend, they dissected the possible mechanism of inhibition of AKT signaling pathway in human neuroblastoma cells. Although they found that some of the key down-stream factors in the pathway viz. Chan et al 79 explored the activity of cucurbitacin B in human hepatocellular carcinoma in vitro and in vivo , where they reported that it caused dose- and time-dependent clonogenic inhibition via STAT3 independent S-phase arrest.

Cucurbitacin B with variable IC 50 value induced cell cycle arrest and cellular differentiation in acute promyelocytic and myeloid leukemia It induced S phase growth arrest, swollen morphology of cells, altered cytoskeleton due to rapid and haphazard polymerization of filamentous actin into globular aggregates, and decreased clonogenicity in the immature blasts. Similar findings were noted in human leukemic Jurkat cells Cucurbitacin B caused cofilin dephosphorylation and actin dynamics intrusion, prompting cell volume increase and simultaneous multi-nucleation.

It also induced autophagosomes and LC3II upregulation as a compensatory protective response. Constitutive suppression of autophagy led to dramatic increase in caspase-3 mediated autophagy. Gao et al 84 reported the anticancer effects of cucurbitacin B in prostate cancer cells. Cucurbitacin B caused selective toxicity in human epithelial type prostate cancer cells. ACLY is an enzyme, which metabolically converts mitochondrial citrate into acetyl coenzyme A 85 , Acetyl coenzyme A is a major precursor and constituent responsible for synthesis of fatty acids and mevalonate, which promote carcinogenesis.

Cucurbitacin B downregulated the expression of acetyl coenzyme A, fatty acid synthesis and mevalonate, supplemented with mitochondrial ROS production. It was suggested that the inhibition of the acetyl coenzyme A signaling might be one of the downstream mechanisms of ROS-mediated intracellular insults leading into apoptosis.

This was supported with downregulation of cyclin B1, phospho-STAT3 and BCL2, associated with chromatin condensation, nuclear fragmentation, and appearance of apoptotic bodies in a dose- and time-dependent manner. It suppressed the expression of cyclin D1, cyclin E, CDK4 and CDK2 and upregulated the expression of p27, all of which are indicated in inhibition of cell cycle progression. Cucurbitacin B was shown to cause cytotoxicity to a variety of bone cancer and normal cells at nanomolar doses Ma et al 92 monitored hypoxia-induced signaling and modulation by cucurbitacin B in various cell lines in vitro.

Contemporary treatment with a known proteasomal inhibitor MG overshadowed the hypoxia signaling suppression, implying that cucurbitacin B did not affect transcriptional coding, but regressed its ubiquitin-mediated proteasomal degradation. It also altered microtubule structures in human cervical cancer HeLa and osteosarcoma U-2OS cells Zhang et al 94 showed that cucurbitacin B induced caspase-independent autophagy reflux in a variety of cell lines. It suppressed cell growth and proliferation, and inhibited interleukin-6 mediated phosphorylation of STAT3 in a dose-dependent manner.

It induced autophagy as evidenced by appearance of autophagosomes and upregulation of lipidated LC3 II. However, inhibition or knockdown of ATG5 and Beclin1 proteins did not rescue the cells from death. Instead, it forced cells to undergo caspase-dependent apoptosis, suggesting a competitive cross-relation between autophagy and apoptosis.

Cucurbitacin B and its derivatives have shown synergism with other anticancer agents reviewed in Table III. Cucurbitacin B 20 mg was made to react with p -toluenesulfonyl chloride 34 mg and DABCO 20 mg in dichloromethane ml to obtain tosylated intermediate 20 mg , which was then made to undergo nucleophilic substitution using sodium azide Cisplatin, an inorganic water-soluble platinum complex, reacts with and alters DNA after undergoing hydrolysis to produce crosslinks.

Crosslinks impair DNA replication, and forces the cells into G 2 phase arrest. Irinotecan is a topoisomerase inhibitor. Paclitaxel is a cyclodecane isolated from the bark of Taxus brevifolia. It stabilizes microtubules when they are in polymerized form, which causes cell death. In combination with either one of three accomplices, DACE 0. Efficacy in combination with cisplatin has also been checked in cutaneous squamous cell carcinoma Cucurbitacin B 0.

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The combination synergistically downregulated cyclin B1 and CDC2 expressions, with reduction in migratory and invasive potential of the cells. In laryngeal squamous cell carcinoma, the combination 0. In ovarian cancer, cucurbitacin B sensitized cells to cisplatin These effects afforded by the combination had cucurbitacin B at the dose of just a fourth of its IC Treatment was well tolerated by the animals and no evident damage in liver and kidneys was observed. Docetaxel is a microtubule inhibitor. It prevents formation of microtubules leading to failure of growth and cell division. Gemcitabine, a nucleoside metabolic inhibitor, prevents the synthesis of genetic element, hence preventing DNA replication.

However, even with combination, but at only high dose, myelosuppression, hepatotoxicity and leukopenia with gemcitabine combination was encountered. Thoennissen et al reported synergism of cucurbitacin B with gemcitabine in pancreatic cancer. The same group in another study in showed that this combination also inhibited BCL2 and cMYC adding up to apoptosis in pancreatic cancer cells in vitro. These effects were positively validated in vivo with only mild toxicity Protein kinase activity is crucial for a majority of intra-cellular signaling pathways.

Prevention of protein kinase results into cell growth arrest. Gefitinib is a protein kinase inhibitor and known to be orally active selective inhibitor of EGFR, which inhibits autophosphorylation of intracellular tyrosine residues. Cucurbitacin B at safe dose 0. Thymidylate is one of the important building blocks of DNA. Its synthesis is mainly stimulated by tetrahydrofolate.

Methotrexate, an antineoplastic antimetabolite with immunosuppressant properties, is an inhibitor of tetrahydrofolate dehydrogenase. Further in vivo validation exhibited tumor suppression by combination cucurbitacin B at 0. Doxorubicin, a topoisomerase inhibiting anthracycline, intercalates DNA and exerts its anticancer activity by the suppression of DNA polymerase, topoisomerase II, and methyltransferase Doxorubicin-resistant cells are known to entail survivin super-expression In a recent study, cucurbitacin B up to 0.

It also induced cofilin dephosphorylation and caspase-mediated apoptosis. Valproic acid, popular anti-convulsion and mood stabilizing fatty acid, is inhibited by histone deacetylase drug resistance. Histone deacetylase activates tumor suppressors p53, p21 and CDKs, and increase histone acetylation, which suppress the activation of many proto-oncogenes Cucurbitacin B caused dose-dependent toxicity in mouse melanoma cells, followed by multiploidy, autophagy and BCL2 upregulation for cell survival When administered in combination with valproic acid 1—5 mM , it showed synergism to sensitize the cells to the toxicity due to valproic acid.

It henceforth caused cell apoptosis and tapered multiploidization. Curcumin, obtained mainly from Curcuma longa , a yellow-orange phytopolyphenolic pigment commonly known as turmeric, is known for its medicinal properties such as anti-oxidant prevention of ROS production , anti-inflammatory COX inhibition and anticancer suppression of protein kinase C. It fundamentally operates via mitochondrial invasion and is relatively safe to the healthy tissue Combination of cucurbitacin B It decreased the sensitivity of the cells to P-glycoprotein and reversed the resistance to 5-fluorouracil, indicating reversal of multidrug resistance.

Cucurbitain B in combination with glycosides exhibited excellent antioxidant properties in a dose-dependent manner Further augmentation with irradiation resulted in rapid cell death. Cucurbitacins, Picracin and deacetylpicracin from Picrorhiza scrophulariiflora inhibited mitogen-induced T cell proliferation and IL-2 Authors regarded picracin as more active in inducing apoptosis of non-stimulated T cells than the others.

Potential of cucurbitacin B against cardiac, liver, lung, neuronal and skin injuries, systemic infections, inflammation, sex-related behavior and adipocyte differentiation has also been explored. Cucurbitacins exhibit a broad range of pharmacological properties such as anti-inflammatory, antioxidant, antiviral, antipyretic, analgesic and anti-malarial — Cucurbitacin B fed mice demonstrated a significant reduction in heart weight, myocardial cell cross sectional area and interstitial fibrosis.

Cucurbitacin B may be indicated in sepsis-induced acute lung injury ALI A rat ALI model following abdominal septic puncture was treated with cucurbitacin B intraperitoneally. Cucurbitacin B-treated rats showed an increase in arterial oxygen partial pressure, and reduction in lung effusion, protein content, neutrophils and lymphocytes, and cytokines in a dose-dependent manner, with 3- to 5-fold increment in survival. Histological examination revealed that the pulmonary destruction was alleviated with cucurbitacin B treatment, endorsing its anti-oxidant and anti-inflammatory properties.

Cucurbitacin B offered hepatoprotective and anti-inflammatory effects in artificially induced acute liver damage in outbred albino male Wistar rats However, higher dose showed signs of irreversible hepatotoxicity. It is characterized by hyperproliferation, inflammation and abnormal keratinocyte differentiation. Imiquimod is an analog of adenosine, a chemical stress inducer. Topical application of cucurbitacin B inhibited imiquimod-induced pathogenesis of psoriatic dermatitis Yesilada et al 42 indexed anti-inflammatory property of cucurbitacin B using Whittle method, using a fraction from the freeze-dried fruit juice of squirting cucumber Ecballium elaterium.

They estimated dye leakage from the vascular tissue in orally fed mice. Vascular leakage corresponded to permeability and inflammatory response. Likewise, the ameliorative anti-oxidant effects of cucurbitacin B and its relatives were shown as beneficial against the neuronal injury Rawat et al 43 also evaluated the anti-oxidant and anti-inflammatory potential of cucurbitacin B containing plant extracts.

Extracts of cucurbits from L. Cucurbitacun B with cucurbitacin E in the dichloromethanolic extract from the roots of Wilbrandia ebracteata Cogn. Male Wistar rats were injected with inflammatory agent carrageenan in paws, which developed into inflammation. Inflammation was significantly less in rats fed with the extract.

Furthermore, pain felt with acetic acid application in the inflamed area was significantly less as compared to the vehicle group. Cucurbitacin B reduced the likelihood of onset of hepatocellular carcinoma by preventing STAT3 phosphorylation and consequent adipocyte accumulation Seo et al showed that cucurbitacin B suppressed the activation of STAT3, henceforth suppressing adipocyte differentiation and accumulation.

Prevention of adipogenesis and lipid accumulation by 0. Genetic silencing of STAT3 significantly attenuated the anti-adipogenic activity. Cucurbitacin B showed synergistic antibacterial and antiviral potential against Staphylococcus aureus and Herpes simplex virus-1 Within a range of dose, cucurbitacin B in synergism with other antibiotics such as tetracycline and oxacillin inhibited the growth of clinical drug resistant variant of Staphylococcus aureus , as determined by microdilution method and checkboard assay.

By means of plaque number reduction assay, it showed potent anti-HSV-1 potential, comparable to acyclovir. Cucurbitacin B treatment, however, led to decline in the sexual hormone and behavior in male moth Agrotis ipsilon Cause of death was acute pulmonary edema and respiratory arrest. Smit in reported that in rabbits the median lethal dose of cucurbitacin B was 0. Ferguson et al also reported poisoning after human consumption of g of commercially produced Cucurbita pepo L.

Toxic symptoms included bitter taste in mouth, abdominal cramps, diarrhea, and occasional vertigo and syncope. Australian Therapeutic Goods Administration has listed cucurbitacin B free from restricted use and encourages its use in combination with other agents Deaths at this dose were accompanied with symptoms such as pulmonary edema, however, with no mention of additional symptoms. Furthermore, severe toxicity leading to death following oral administration were reported in various studies reporting the use of plant and extracts - Ecballium elaterium in rabbits caused nervousness, restlessness, seizures, anorexia, tachycardia, tachypnea, dyspnea, cyanosis, and diarrhea eventually leading to death , ; Cucurbita texana in Swiss Webster mice caused severe anemia followed by death ; Citrullus colosynthis and Lagenaria siceraria in goats caused restlessness, anorexia, diarrhea, dehydration, anemia, dyspnea, kinetic latency, internal hemorrhages, pulmonary emphysema, enteritis, multi-organ failure, and eventually death ; and Citrullus colocythis in Bovans-type chicks led to hepatic fatty changes and toxicity, catarrhal enteritis, pulmonary emphysema and renal tubular necrosis, but these symptoms reversed after 4 weeks of withdrawal Various human toxicity complaints have been reported from around the world after accidental or intentional consumption of fruit juice of zucchini squash , , Symptoms reported were similar to those in the in vivo studies pivoting digestive and neurological systems.

However, following topical application with the same extract the human subjects remained asymptomatic Since the median lethal dose via oral route was significantly higher than the parenteral, possibly digestion, emergence of metabolites and their absorption from the gut before reaching systemic circulation is crucial to alleviate its toxic effects and liberate its medicinal potency.

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Moreover, oral feeding led toxicities and deaths involved components additional to cucurbitacin B, advocating bail for cucurbitacin B off severely toxic profile. Therefore, oral administration of purified form of cucurbitacin B as an independent executor may be justified, as long as the dosage is conscientiously tailored and the symptoms are cautiously checked. The natural origin and synthetic production of cucurbitacin B have been extensively studied over the last few decades.

Jung and Lui presented the artificial convergent edifice efforts.

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Razavilar and Choi found that the diffusivity of cucurbitacin B depends on wiggling motion of the block copolymers to diffuse while the contemporaneous water molecules diffusion via a hopping mechanism. Toker et al proposed a novel method to naturally increase the yield of cucurbitacin B using Ecballium elaterium callus culture technique. Mei et al suggested a process for cucurbitacin B bioproduction from one of its parent glycoside using a specific Streptomyces sp. The process was mild, simple and prolific; nevertheless, its hydrophobic and electrostatic structure left it prognostically difficult.

Quick exploitation followed by attenuated performance of cucurbitacin B may abete solid doubts about the treatment modality and dosage in practical use. Cucurbitacin B is hydrophobic, hence suffers in situ absorption. Its absorption from carboxymethyl chitosan films loaded with phospholipid-bile salt-mixed micelles as mucoadhesive buccal films resulted in 2. Cheng et al prepared berberine hydrochloride modified phospholipid complex loaded cucurbitacin B CUB-PLC-BER as a formulation and tested its delivery and efficacy against cholangiocarcinoma in Berberine hydrochloride is known to stimulate bile release, hence was believed to contribute to sustained and prolonged drug release.

Cucurbitacin B loaded with phospholipids and berberine hydrochloride had higher drug delivery rate, and was more cytotoxic to the cancer cells in both in vitro and in vivo. Wang et al encapsulated cucurbitacin B in glycosylated solid lipid nanoparticles. You et al predicted the direct relation between the STAT3 protein localization and autophagy.

Cytoplasmic localization initiated direct protein-to-protein interaction and impeded autophagy by countervailing autophagy related proteins. It is mediated at the genetic level where STAT3 activation may prompt genetic remodeling and attenuation of autophagy.


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Mitochondrial translocation of STAT3 constitutively suppressed autophagy. Studies reported that cucurbitacin B and derivatives interfered with the activation of STAT3 61 , 63 , 74 , 82 , 87 , 88 , 94 , 95 , 98 , 99 , — , , , , Autophagy signaling is a fairly new subject. Cucurbitacin B and its role in autophagy is mostly unexplored, hence the field is wide blank to fill in.

Cucurbitacins, steroids derived from triterpene hydrocarbon, found in a number of plant families, are some of the principle compounds, which attribute medicinal qualities to the plant. Cucurbitacin B, the bitter toxin, in previous few decades has splendidly verified its cytotoxic potential against cancer and other medical conditions. Through various mechanisms, it suppressed the pathogenesis and inhibited the spread of cancer in vitro and in vivo Figs.

Treatment with cucurbitacin B consistently upregulated DNA damage and pro-apoptotic protein markers, while downregulated pro-survival markers, growth receptors and cell cycle progressors at either transcriptional level or via their ubiquitination and proteasomal degradation. Consequently, it caused growth arrest, apoptosis, cellular differentiation, and inhibition of proliferation in cancer cells.

It also showed significant efficacy against the developing detrimental effects of cardiac, pulmonary, neurological and hepatic injuries, psoriasis, infections and lipogenesis. It also caused STAT3 dependent autophagy. Bio-production, efficacy and metabolism of the compound may be improved by means of slight chemical modulation such as the use of hydroponics, bio-transformers, micelles and nanomaterials.

It is not difficult to categorize cucurbitacin B as an effective anticancer molecule. It has the potential to prevent cancer, delay its progression, and might be able to completely cure it. Since it is procured from the natural sources, it could significantly economize the expenditure against the continuously growing disease. Surprisingly, not one human study to explore the efficacy of the molecule has been conducted so far.

Clinical trials for cucurbitacin B as the mainline-targeted anticancer therapy either as an independent effector or as a supplement is warranted. Cancer Research UK. Accessed June 20, Curr Opin Cell Biol. Sci Signal. Hengartner MO: The biochemistry of apoptosis. Korenjak M and Brehm A: E2F-Rb complexes regulating transcription of genes important for differentiation and development. Curr Opin Genet Dev. Cancer Res.

Cucurbitacin B and cancer intervention: Chemistry, biology and mechanisms (Review)

EMBO J. J Cell Biochem. View Article : Google Scholar. Curr Cancer Drug Targets. World J Gastroenterol. Clin Cancer Res. Mol Cancer. PLoS One. Mol Pathol. Adv Cancer Res. Acta Pharmacol Sin. Harley CB: Aging of cultured human skin fibroblasts. Methods Mol Biol. Hayflick L: The limited in vitro lifetime of human diploid cell strains. Exp Cell Res. Cell Metab. Herbal Medicine: Biomolecular and Clinical Aspects. Pharmacogn Rev. Alghasham AA: Cucurbitacins - a promising target for cancer therapy.

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