condition found tbRes List
Bos, Boswellia (frankincense): Click to Expand ⟱
Features:
Boswellia is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.
May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.
-Naturally occurring pentacyclic triterpenoids include ursolic acid (UA), oleanolic acid (OA), betulinic acid (BetA), bosewellic acid (BA), Asiatic acid (AA), α-amyrin, celastrol, glycyrrhizin, 18-β-glycyrrhetinic acid, lupeol, escin, madecassic acid, momordin I, platycodon D, pristimerin, saikosaponins, soyasapogenol B, and avicin
Boswellia refers to a group of resinous extracts obtained from Boswellia trees (e.g., Boswellia serrata). Traditionally used in Ayurvedic and traditional Chinese medicine, Boswellia is reputed for its anti-inflammatory, analgesic, and immunomodulatory properties. Its bioactive components—such as boswellic acids.
-Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase) 5LOX↓,.
-AKBA used to reduce Methionine ***** (help in Methionine reduced diet)
Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day

AKBA (Acetyl-11-keto-β-boswellic acid) is a bioactive compound derived from Boswellia serrata, a plant used traditionally for its anti-inflammatory properties. (upto 30% AKBA in Boswellia MEGA AKBA)
AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)

-Note half-life reports vary 2.5-90hrs?.
BioAv
Pathways:
- induce or lower ROS production (not consistant increase for cancer cells)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, VEGF↓, NF-κB↓, CXCR4↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, TOP1↓,
- inhibits angiogenesis↓ : VEGF↓, Notch↓, PDGF↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells


CDK4, Cyclin-dependent kinase 4: Click to Expand ⟱
Source:
Type:
Cyclin-dependent kinase 4 (CDK4) is a key regulator of the cell cycle, particularly in the transition from the G1 phase to the S phase. Its expression and activity are often altered in various cancers, contributing to tumorigenesis.
CDK4 is frequently overexpressed in various cancers, and its expression levels can serve as a prognostic marker.
Scientific Papers found: Click to Expand⟱
2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoP↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

1450- Bos,  Cisplatin,    3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells
- in-vitro, Pca, DU145
ROS↑, increased reactive oxygen species (ROS) generation
MMP↓,
Casp↑,
Apoptosis↑,
Bax:Bcl2↑,
TumCCA?, induce G0/G1 arrest
cycD1↓,
CDK4↓,
P21↑,
p27↑,
NOTCH↓, AKBA demonstrated significant downregulation of Notch signaling mediators
ChemoSen↑, AKBA has the potential to synergistically enhance the cytotoxic efficacy of cisplatin

1427- Bos,    Acetyl-keto-β-boswellic acid inhibits cellular proliferation through a p21-dependent pathway in colon cancer cells
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, CRC, LS174T
TumCG↓,
TumCCA↑, G1 phase
cycD1↓,
cycE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
P21↑,

1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Results for Effect on Cancer/Diseased Cells:
5HT↓,1,   angioG↓,1,   AntiCan↑,1,   Apoptosis↑,2,   AR↓,1,   ascitic↓,1,   BAX↑,1,   Bax:Bcl2↑,1,   Bcl-2↓,1,   BioAv↓,1,   BioAv↑,2,   Casp↑,1,   Casp3↑,1,   Casp8↑,1,   CDK2↓,2,   CDK4↓,4,   CDK6↓,1,   chemoP↑,1,   ChemoSen↑,3,   cMyc↓,1,   COX2↓,1,   CXCR4↓,1,   cycD1↓,4,   cycE↓,2,   Dose↑,1,   DR4↑,1,   DR5↑,1,   eff↑,4,   p‑ERK↓,1,   Half-Life↓,1,   IKKα↓,1,   IL1α↓,1,   Let-7↑,1,   lipid-P?,1,   MCP1↓,1,   MIP2↓,1,   miR-200b↑,1,   miR-27a-3p↓,2,   miR-34a↑,2,   MMP↓,1,   MMP1↓,1,   MMP2↓,1,   MMP9↓,1,   NF-kB↓,1,   NOTCH↓,1,   P21↑,2,   p27↑,1,   cl‑PARP↑,1,   PARP1↓,1,   PDGF↓,1,   p‑PDGFR-BB↓,1,   PPARα↓,1,   p‑RB1↓,2,   ROS↑,1,   STAT3↓,1,   Tf↓,1,   TOP1↓,1,   TOP2↑,1,   toxicity↓,1,   TumCCA?,1,   TumCCA↑,2,   TumCG↓,2,   TumCI↓,1,   VEGF↓,2,   Wnt↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 66

Results for Effect on Normal Cells:
Ca+2↝,1,   Inflam↓,1,   MAPK↑,1,   NF-kB↓,1,   TNF-α↓,1,  
Total Targets: 5

Scientific Paper Hit Count for: CDK4, Cyclin-dependent kinase 4
4 Boswellia (frankincense)
1 Cisplatin
1 Curcumin
1 Chemotherapy
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:47  Target#:894  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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