Copyright ©The Author(s) 2021.
World J Biol Chem. Mar 27, 2021; 12(2): 15-37
Published online Mar 27, 2021. doi: 10.4331/wjbc.v12.i2.15
Table 1 Marine compounds with potential anticancer activity against breast cancer from microorganisms and algae
Marine compound
Chemical nature
Mechanism of action
Gallic acid (GA)Phenolic compound(1) Altered the expression of P53, Mcl and p21 as well as cell cycle regulators; and (2) MAP38 kinase involved in GA induced cell cycle arrest and apoptosis via downregulating cyclin Da/CDK4 and cyclin E/CDK2Moghtaderi et al[74]
GAPhenolic compound(1) In combination with curcumin stimulated apoptosis by increasing the Bax expression, activating PARP and caspase 3; (2) Decreased Bcl2 expression; and (3) Arrested at sub-G1 stage
GAPhenolic compoundConjugated to Gold NPs, suppressed metastasis by blocking EGF dependent MMP-9 expression via suppressing stabilization of p300 and activation of NF-κB/c-Jun pathwayChen et al[75]
Crambescidin 800Heteropenta cyclic guanidine alkaloidInduced cell cycle at the G2M phase by decreasing the cyclin D1, CDK-4, and -6 expression in TNBC cells via modulating Akt/NF-κB/MAPK pathwayMoon et al[102]
EPS11Polysaccharide(1) Inhibited lung metastasis by inhibiting cell adhesion protein CD99; and (2) Inhibited cancer cell growth by inducing anoikis via inducing Akt pathway-dependent expression of βIII-tubulinCao et al[77]
SWP1 and SWP2PolysaccharideInhibited proliferation by inducing apoptosis, activating caspase 3/9 and disrupting the mitochondrial membrane via generation of ROSVaikundamoorthy et al[78]
CarrageenanPolysaccharideInduced apoptosis via promoting condensation of the nucleus and fragmentation of DNA as well as activating caspase 8, an extrinsic apoptotic proteinMurad et al[79]
ExopolysaccharidePolysaccharide(1) Inhibited the cell growth by decreasing the cyclin D1 and E expression; and (2) Induced the proliferation of B-cells and decreased production of IL-6 and TNF-1α in T-cellsPark et al[80]
Ilmycin CCyclic peptideInhibited migration and invasion by inducing apoptosis via Bax/Bcl-2 dependent caspases as well as inhibiting MMP-2 and -9 via blocking IL-6 dependent phosphorylation of STAT3Xie et al[81]
Inhibited growth by inducing apoptosis through activation of SR stress and reducing Bcl2 in a CHOP dependent mannerZhou et al[82]
MolassamideCyclic depsipeptide(1) Abrogated elastase-dependent migration of highly metastatic TNBC cells; and (2) Inhibited the activity of elastase and the migration of TNBC cells by targeting the expression of ICAM-1 via inhibiting the NF-κB pathwayAl-Awadhi et al[83]
Kempopeptin CCyclic depsipeptideInhibited invasion and migration by decreasing the cleavage of matriptase substrates CDCP1 and sesmoglein-2Al-Awadhi et al[84]
Cyclic leucylprolineCyclic peptideInhibited migration by inhibiting cell proliferation, inducing cell arrest via DNA damage. Mechanistically, CLP induced cell cycle arrest by blocking the expression of cyclin C, CDK4, PAK, RAC1, and p27kiP1 via targeting CD151 and EGFR signaling axis in TNBC cellsKgk et al[85]
GalaxamideCyclic pentapeptideElicited apoptosis in BC cells by arresting at the G1 phase as well as reducing mitochondrial membrane potential via the generation of ROSLunagariya et al[86]
Brintonamide DLinear peptideReduced the CCL27 and stimulated proliferation and progression of metastatic BC cells by targeting serine protease kallikrein 7 (KLK7). This study reported that brintonamide D targeted KLK7 by modulating CCR10, the receptor of CCL27 in BC cellsAl-Awadhi et al[87]
Iturin ALipopeptide(1) Induced apoptosis by increasing sub-G1 cell population, fragmentation of DNA via inhibiting FGF-mediated phosphorylation of Akt, FoxO3a and GSK3β; (2) And reduced tumor growth by promoting translocation of FoxO3a via downregulating MAPK and Akt kinase in the xenograft modelDey et al[88]
Halilectin-3Sugar-binding lectin proteinInhibited proliferation by inducing arrest at the G1 phase and apoptosis by increasing the activity of caspase 9 and autophagy by inducing the expression of light chain 3do Nascimento-Neto et al[89]
SinularinTerpenoidReduced cell viability by halting at the G2M phase and stimulating apoptosis through activation of caspase-3 and -8 as well as PARP. In addition, it also induced DNA damage by generating ROS via stimulating oxidative stressHuang et al[90]
Sipholenol ATriterpeneReduced the metastatic ability of TNBC cells by inhibiting protein tyrosine kinase 6, a key mediator of growth factor-dependent migrationFoudah et al[91]
Agelasine BDiterpene alkaloid(1) Induced apoptosis by inhibiting ER Ca2+ -ATPase (SERCA) activity via releasing Ca2+ from ER and inducing DNA fragmentation; (2) Reduced the Bcl2 expression and enhanced the caspase 8 expression; and (3) Induced cell death in an ER-mediated extrinsic apoptotic pathwayPimentel et al[92]
Hirsutanol ASesquiterpene(1) Reduced cell growth by inhibiting proliferation; (2) Induced apoptosis, and autophagy via generating ROS; and (3) Silenced Atg7 with siRNA and blockade of autophagy using bafilomycin A1 synergistically increased the efficacy of hirsutanol A in inducing apoptosis and inhibiting cell proliferationYang et al[93]
DehydrothyrsiferolTriterpenoidInduced apoptosis by causing DNA fragmentation and arrest at S-phase and G2M phasePec et al[94]
SodwanoneTriterpene(1) Induced cytotoxicity to BC cells; and (2) Inhibited hypoxia-induced HIF-1αDai et al[95]
PseudopterosinDiterpene glycoside (1) Reduced the production of IL-6, TNF-1α, and MCP-1 via blocking p65 and IkB phosphorylation; and (2) Promoted translocation of glucocorticoid receptor from nucleus to cytosolSperlich et al[96]
QuinazolineHeterocyclic compound(1) Induced apoptosis in HER+ve BC cells by reducing the Bcl2 expression and increasing the Bax expression; and (2) Promoted cell death via ROS-dependent extrinsic or intrinsic apoptotic pathways without systemic toxicity in the mouse modelDe et al[97]
(3β)-Cholest-5-en-3-olCholesterolInduced cell death by activating caspase 3 and 8 as well as increasing the Bax expression and decreasing the Bcl2 expressionSharifi et al[98]
3β,11-dihydroxy-9,11-secogorgost-5-en-9-oneSterol(1) Inhibited cell growth by inducing apoptosis via activation of caspase 3 and PARP and cell cycle arrest via targeting cyclin D1 and CDK6 through blocking the p38/ERK signaling pathway; and (2) Induced autophagy via generating ROS and DNA damage by increasing the expression of H2AXWeng et al[99]
4-methyenedioxy-β-nitrostyreneβ-nitrostyrene derivativesInhibited migration by disrupting the focal adhesion complex as well as a network of actin stress fibers via reducing β1 integrin-dependent phosphorylation of FAK and paxillinChen et al[100]