LRP6 Cancer Research Results
LRP6, Low-density lipoprotein receptor–related protein 6: Click to Expand ⟱
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LRP6 (Low-density lipoprotein receptor–related protein 6) is a single-pass transmembrane co-receptor that plays an essential role in the canonical Wnt/β-catenin signaling pathway. Wnt signaling is critically involved in embryonic development, cell proliferation, differentiation, and tissue homeostasis. Dysregulation of this pathway is a well-known contributor to oncogenesis.
LRP6 plays a significant role in the regulation of the Wnt/β-catenin signaling pathway—a key driver in many cancers. Its overexpression is commonly observed in various tumor types and often correlates with an aggressive clinical profile, including poor survival outcomes. These findings not only underscore the importance of LRP6 as a prognostic biomarker but also highlight its potential as a target for novel therapeutic interventions.
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Scientific Papers found: Click to Expand⟱
E-cadherin↑,
ZO-1↑,
Zeb1↓,
N-cadherin↓,
Vim↓,
Snail↓,
Slug↓,
MMP2↓,
MMP9↓,
TumCMig↓,
TumCI↓,
LRP6↓,
p‑LRP6↓,
β-catenin/ZEB1↓,
TumVol↓, in vivo
TumW↓,
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in-vitro, |
BC, |
SUM159 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
HS587T |
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in-vitro, |
BC, |
BT549 |
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Wnt↓, HT suppressed Wnt/ß-catenin signaling by decreasing p-LRP6, LRP6, ß-catenin and cyclin D1 protein expression and the EMT markers SLUG, ZEB1, SNAIL and VIMENTIN.
β-catenin/ZEB1↓,
LRP6↓,
cycD1/CCND1↓,
EMT↓,
Slug↓,
Zeb1↓,
Snail↓,
Vim↓,
TGF-β↓, correlated with a less TGFß activity.
CSCs↓, we report for the first time the inhibitory role of HT on BCSCs and tumor cell migration by targeting EMT, Wnt/ß-catenin and TGFß signaling pathways.
TumCMig↓,
chemoP↑, chemopreventive compound HT as a novel candidate to be investigated as an alternative targeted therapy for TNBC.
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
BT549 |
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in-vitro, |
BC, |
SUM159 |
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CSCs↓, HT reduced BCSCs self-renewal, ALDH+ (aldehyde dehydrogenase) and CD44+/CD24-/low subpopulations, tumor cell migration and invasion.
TumCMig↓,
TumCI↓,
β-catenin/ZEB1↓, HT suppressed Wnt/β-catenin signaling by decreasing p-LRP6, LRP6, β-catenin and cyclin D1 protein expression and the EMT markers SLUG, ZEB1, SNAIL and VIMENTIN.
Wnt↓,
p‑LRP6↓,
LRP6↓,
cycD1/CCND1↓,
EMT↓,
Slug↓,
Zeb1↓,
Snail↓,
Vim↓,
SMAD2↓, Finally, HT inhibited p-SMAD2/3 and SMAD2/3 in SUM159PT, BT549 and MDA-MB-231 cells, what was correlated with a less TGFβ activity.
SMAD3↓,
TGF-β↓,
Wnt/(β-catenin)↓,
ALDH1A1↓,
LRP6↓,
TumCP↓, Niclosamide was found to inhibit adrenocortical carcinoma cellular proliferation, which was associated with apoptosis, reduction of epithelial-to-mesenchymal transition and β-catenin levels.
Apoptosis↑,
EMT↓,
β-catenin/ZEB1↓,
TumCG↓, Oral administration of niclosamide led to tumor growth inhibition with no observed toxicity.
toxicity↓,
Wnt↓, Lu et al. reported that niclosamide inhibits Wnt/β-catenin signaling by promoting Wnt co-receptor LRP6 degradation in breast cancer cells [11].
LRP6↓,
eff↑, niclosamide acts synergistically with a monoclonal antibody that specifically activates TRAIL death receptor 5 to inhibit tumor growth of basal-like breast cancers [12].
DR5↑,
mTORC1↓,
pH↓, Niclosamide lowered the cytoplasmic pH and may indirectly lead to inhibition of mTORC1 signaling [13]
CSCs↓, Niclosamide also was found to prevent the conversion of non-breast cancer stem cells into cancer stem cells
IL6↓, This mechanism is associated with inhibition of the IL6-JAK1-STAT3 signal transduction pathway
JAK1↓,
STAT3↓, Ren et al. identified niclosamide as a potent STAT3 inhibitor able to suppress STAT3 transcriptional activity
ChemoSen↑, niclosamide alone or in combination with cisplatin represses the growth of xenografts of cisplatin-resistant triple-negative breast cancer cells.
TumCG↓, Niclosamide inhibited growth of colon cancer cells from human patients both in vitro and in vivo, regardless of mutations in APC [24].
tumCV↓, niclosamide selectively inhibited glioblastoma cell viability [29]. Detailed mechanism studies revealed that niclosamide suppressed the Wnt, Notch, mTOR, and NF-κB signaling pathways.
NOTCH↓,
NF-kB↓,
EGFR↓, Li et al. reported that inhibition of EGFR by erlotinib, an FDA-approved therapeutic agent, led to activation of STAT3 signaling in head and neck cancer cells
ROS↑, niclosamide inhibits TNF-α-induced NF-κB–dependent reporter activity and increased the levels of reactive oxygen species (ROS) in AML cells.
RadioS↑, niclosamide enhanced radiosensitivity of the non-small cell lung cancer cell line H1299.
cFos↓, inhibit osteosarcoma cell proliferation, migration, and survival. This inhibitory effect is associated with decreased expression of c-Fos, c-Jun. E2F1, and c-Myc.
cJun↓,
E2Fs↓,
cMyc↓,
Half-Life↓, Niclosamide exhibits a short half-life (6.0 ± 0.8 h). Niclosamide was rapidly absorbed with a Tmax of less than 30 min. The Cmax is 354 ± 152 ng/mL.
BioAv↝, AUC and bioavailability were 429 ± 100 and 10%, respectively. In order to make more effective use of niclosamide, additional work needs to be done to improve its solubility, absorption and systemic bioavailability.
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
DU145 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
Nor, |
HEK293 |
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Wnt↓, salinomycin was not only a potent Wnt/β-catenin signaling inhibitor, bus also a strong mTORC1 signaling antagonist in breast and prostate cancer cells.
β-catenin/ZEB1↓,
mTORC1↓, SALINOMYCIN INHIBITS MTORC1 SIGNALING IN BREAST AND PROSTATE CANCER CELLS
GSK‐3β↑, Mechanistically, salinomycin activated GSK3β in cancer cells.
cycD1/CCND1↓, salinomycin was able to suppress the expression of cyclin D1 and survivin, two targets of both Wnt/β-catenin and mTORC1 signaling, in prostate and breast cancer cells,
survivin↓,
LRP6↓, SALINOMYCIN INHIBITS LRP6 EXPRESSION AND WNT/β-CATENIN SIGNALING IN BREAST CAND PROSTATE CANCER CELLS
TumCG↓, SALINOMYCIN INHIBITS BREAST AND PROSTATE CANCER CELL GROWTH AND INDUCES CANCER CELL APOPTOSIS
Apoptosis↑,
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1,
Cell Death ⓘ
Apoptosis↑, 2, DR5↑, 1, survivin↓, 1,
Transcription & Epigenetics ⓘ
cJun↓, 1, tumCV↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 3, E2Fs↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ALDH1A1↓, 1, cFos↓, 1, CSCs↓, 3, EMT↓, 3, GSK‐3β↑, 1, LRP6↓, 6, p‑LRP6↓, 2, mTORC1↓, 2, NOTCH↓, 1, STAT3↓, 1, TumCG↓, 3, Wnt↓, 4, Wnt/(β-catenin)↓, 1,
Migration ⓘ
E-cadherin↑, 1, MMP2↓, 1, MMP9↓, 1, N-cadherin↓, 1, Slug↓, 3, SMAD2↓, 1, SMAD3↓, 1, Snail↓, 3, TGF-β↓, 2, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 1, Vim↓, 3, Zeb1↓, 3, ZO-1↑, 1, β-catenin/ZEB1↓, 5,
Angiogenesis & Vasculature ⓘ
EGFR↓, 1,
Immune & Inflammatory Signaling ⓘ
IL6↓, 1, JAK1↓, 1, NF-kB↓, 1,
Cellular Microenvironment ⓘ
pH↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 1, ChemoSen↑, 1, eff↑, 1, Half-Life↓, 1, RadioS↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
chemoP↑, 1, toxicity↓, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 54
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: LRP6, Low-density lipoprotein receptor–related protein 6
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#:% Target#:1005 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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