Hops (Humulus lupulus) / TumCI Cancer Research Results

Hops, Hops (Humulus lupulus): Click to Expand ⟱
Features:
Hops (Humulus lupulus) – Hops (known for beer brewing) contain compounds like xanthohumol that have demonstrated anticancer activity, particularly in breast and prostate cancer.
-Phytochemicals, including flavonoids and polyphenols, which have antioxidant properties.
-8-prenylnaringenin, may have estrogenic effects. (Hormone related cancers)
-Anti-inflammatory properties
Dose: Tea 1-3g/d, 1-3x/d. Extract 300-500mg/d

Hops (Humulus lupulus) — the dried female inflorescences or hop cones of Humulus lupulus L., a perennial plant in the Cannabaceae family, are a complex botanical mixture containing prenylated flavonoids, polyphenols, α- and β-bitter acids, proanthocyanidins and volatile terpenes. Hops are classified as a botanical/natural-product mixture; the recommended abbreviation is Hops or HL. This entry represents whole hops and hop extracts rather than purified xanthohumol, which has substantially stronger and more specific anticancer evidence and is appropriately maintained as a separate product. Extract composition varies markedly with cultivar, processing and extraction method, so biological effects cannot be assumed to be uniform across commercial hop preparations.

Primary mechanisms (ranked):

  1. Suppression of tumor invasion and migration by polyphenol-rich spent-hop extract, associated with reduced MMP-2 and MMP-9 expression and activity.
  2. Antiangiogenic activity through reduced HIF-1α and VEGF expression in colorectal cancer cells.
  3. Modulation of carcinogenic estrogen metabolism, including suppression of CYP1A1/CYP1B1 induction, reduced estradiol 4-hydroxylation and inhibition of estrogen-induced malignant transformation in mammary epithelial cells.
  4. Anti-inflammatory signaling, including reduced NF-κB activity, COX-2, iNOS and inflammatory cytokines such as IL-6 in experimental hop-extract models.
  5. Direct antiproliferative effects have been reported for some whole or spent-hop extracts in colorectal and other cancer-cell models, but these effects are less extensively characterized than those of isolated hop constituents.
  6. Estrogen-receptor modulation is constituent- and preparation-dependent because hop extracts can contain the potent phytoestrogen 8-prenylnaringenin; whole-hop preparations therefore cannot be categorized simply as estrogen suppressive.

Bioavailability / PK relevance: Whole-hop extracts do not have a single definable pharmacokinetic profile because their constituent concentrations and extraction ratios vary substantially. Human studies with standardized hop preparations demonstrate systemic absorption of prenylated hop phenols, including 8-prenylnaringenin and isoxanthohumol-derived metabolites, with considerable inter-individual variability. Gut microbial conversion of isoxanthohumol to 8-prenylnaringenin can materially influence estrogenic exposure. Pharmacokinetic results from one standardized extract should therefore not be generalized to teas, beer, spent-hop extracts or unrelated commercial hop supplements.

In-vitro vs systemic exposure relevance: The strongest whole-extract cancer studies are concentration-driven in-vitro experiments. For example, spent-hop extract produced pronounced inhibition of colorectal-cancer invasion and migration at approximately 200 µg/mL, whereas estrogen-metabolism effects have been reported at lower extract concentrations such as 5 µg/mL. Whether these concentrations and phytochemical ratios are achieved in human tumors after conventional oral hop supplementation is unknown. Direct systemic anticancer exposure from ordinary dietary hops or beer should not be assumed equivalent to experimental extracts.

Clinical evidence status: Preclinical for cancer. Whole-hop and spent-hop extracts have demonstrated chemopreventive, anti-invasive, antiangiogenic and estrogen-metabolism effects in cell and animal models, but there is no established randomized clinical evidence that whole hops treat human cancer. Human hop-extract trials have primarily evaluated menopausal symptoms, sleep, metabolic effects, joint health, safety and pharmacokinetics rather than oncology efficacy. Hops are used as traditional herbal products for mild stress and sleep-related indications in European regulatory monographs, not for cancer treatment.

Hops Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 MMP-2 and MMP-9 Invasion Axis ↓ MMP-2
↓ MMP-9
↓ invasion
↓ migration		 ↔ / unclear G Reduced metastatic phenotype Demonstrated with polyphenol-rich spent-hop extract in SW-480 and HT-29 colorectal cancer cells. Strong inhibition required relatively high extract concentrations.
2 HIF-1α VEGF Angiogenesis ↓ HIF-1α
↓ VEGF
↓ angiogenic signaling		 ↓ pathological endothelial response (context-dependent) G Antiangiogenic activity Spent-hop extract reduced HIF-1α and VEGF expression in colorectal cancer models and inhibited angiogenesis-related behavior.
3 Estrogen Oxidative Metabolism ↓ CYP1B1
↓ CYP1A1 induction
↓ estradiol 4-hydroxylation		 ↓ estrogen-induced malignant transformation G Reduced formation of potentially genotoxic estrogen metabolites A standardized hop extract inhibited oxidative estrogen metabolism and estrogen-induced transformation in MCF-10A mammary epithelial cells. This is primarily chemopreventive rather than evidence of tumor treatment.
4 NF-κB Inflammatory Signaling ↓ inflammatory signaling (context-dependent) ↓ NF-κB
↓ inflammatory response		 R-G Anti-inflammatory activity Best characterized with polyphenol-rich spent-hop extract in activated macrophage and inflammatory models rather than directly in cancer cells.
5 COX-2 iNOS and Cytokines ↓ inflammatory tumor-supportive signaling (context-dependent) ↓ COX-2
↓ iNOS
↓ IL-6		 R-G Reduced inflammatory mediator production Spent-hop extract markedly reduced COX-2 and IL-6 expression in LPS-activated macrophages. Cancer relevance is primarily through modulation of inflammatory microenvironment mechanisms.
6 Cell Proliferation ↓ proliferation (extract-dependent) Less affected in limited comparative studies G Growth inhibition Reported for spent-hop and other hop extracts, particularly in colorectal cancer models, but potency and composition vary substantially among extracts.
7 Estrogen Receptor Activity ↑ / ↓ ER signaling (constituent-dependent) ↑ estrogenic signaling possible R-G Mixed estrogenic modulation Whole hops contain 8-prenylnaringenin, a potent phytoestrogen. Estrogenic activity depends strongly on extract composition, dose and conversion of isoxanthohumol to 8-prenylnaringenin. Do not classify whole hops simply as ER inhibition.
8 Clinical Translation Constraint Extract-dependent effects
high experimental concentrations frequently required		 Estrogenic exposure is formulation-dependent G Limits oncology translation Whole-hop preparations vary in polyphenols, bitter acids and prenylated flavonoids. Human anticancer efficacy has not been established, and pharmacokinetic equivalence among experimental extracts and commercial products is unknown.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr
TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
7469- Hops,    CHEMOPREVENTIVE PROPERTIES OF SPENT HOPS (HUMULUS LUPULUS L.) EXTRACT AGAINST ANGIOGENESIS, INVASION AND MIGRATION OF COLORECTAL CANCER CELLS
- in-vitro, CRC, SW48 - in-vitro, CRC, HT29
angioG↓, TumCI↓, TumCMig↓, MMP2↓, MMP9↓, VEGF↓, Hif1a↓, chemoPv↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,  
Total Targets: 8

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:220  Target#:324  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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