This 2008 paper gives Phellinus linteus a real but narrow breast-cancer cell-culture signal. A commercial aqueous extract slowed growth mostly through cytostatic S-phase arrest, reduced adhesion, migration, invasion, uPA, endothelial tube formation, and VEGF, and lowered AKT phosphorylation in MDA-MB-231 cells. It does not identify the active molecule or show that the same effect happens in breast tumors in animals or people.
Readers researching Cancer Oncology.
0.25 / 0.5 / 1.0 mg/mLExtract dose ladder These are the main concentrations that anchor the proliferation and invasion phenotype story across the paper.
What the researchers found
The intervention is not a purified polysaccharide or isolated mushroom compound. It is a commercial aqueous Phellinus linteus extract with no batch chemistry or active-fraction analysis in the paper.
PL suppressed breast-cancer growth more than cell viability, especially in the 72-hour 1.0 mg/mL lane, which makes the main growth claim more cytostatic than directly cytotoxic.
The MDA-MB-231 cell-cycle result is not generic arrest language. The paper shows a specific S-phase build from 27% to 34% and 44% with p27 upregulation and without a matching apoptotic sub-G0 or G1 spike.
The anti-invasive lane is broader than a single migration assay, because adhesion, migration, invasion, and uPA secretion all move down together in the invasive MDA-MB-231 model.
The angiogenesis story is meaningful but capped. Direct PL exposure, PL-conditioned media, lower VEGF secretion, and lower p-AKT all point in the same direction, yet the conditioned-media lane remains partly confounded because the authors say they could not remove PL from that media.
This 2008 paper gives Phellinus linteus a real but narrow breast-cancer cell-culture signal. A commercial aqueous extract slowed growth mostly through cytostatic S-phase arrest, reduced adhesion, migration, invasion, uPA, endothelial tube formation, and VEGF, and lowered AKT phosphorylation in MDA-MB-231 cells. It does not identify the active molecule or show that the same effect happens in breast tumors in animals or people.
Why it matters
The second framing is the careful one. The paper is useful because several malignant phenotypes move together in culture, not because it proves breast-cancer treatment efficacy. This 2008 paper gives Phellinus linteus a real but narrow breast-cancer cell-culture signal. A commercial aqueous extract slowed growth mostly through cytostatic S-phase arrest, reduced adhesion, migration, invasion, uPA, endothelial tube formation, and VEGF, and lowered AKT phosphorylation in MDA-MB-231 cells. It does not identify the active molecule or show that the same effect happens in breast tumors in animals or people.
In the RethinkMushrooms taxonomy, this study sits closest to Cancer Oncology. Evidence level: This is materially stronger than a single readout extract paper because it lines up growth, colony formation, invasion, endothelial morphogenesis, VEGF secretion, and AKT signaling in one system. The main weaknesses are material uncertainty and translation: the extract is not chemically standardized, most outcomes are presented as figure-driven dose responses rather than exact endpoint tables, and there is no breast-cancer animal model.. Do not present this as in-vivo breast-cancer efficacy. The paper never tests tumors in mice or humans.
The numbers in context
Extract dose ladder: 0.25 / 0.5 / 1.0 mg/mL. These are the main concentrations that anchor the proliferation and invasion phenotype story across the paper.
MDA-MB-231 24-hour proliferation drop: 15.5% / 21.5% / 43.1%. At 24 hours, the highly invasive breast-cancer line shows a clear but moderate early growth drop across the 0.25 / 0.5 / 1.0 mg/mL range.
MCF-7 24-hour proliferation drop: 60.2% / 70.1% / 78.0%. The lower-invasiveness MCF-7 line was more growth-sensitive than MDA-MB-231 at the same 24-hour doses.
Cytostatic gap at 72 hours: 13.5% vs 86.6%. At 1.0 mg/mL in MDA-MB-231 cells, viability loss stayed small while proliferation suppression was large, which is the paper's cleanest cytostatic-versus-cytotoxic split.
S-phase expansion: 34% and 44%. At 0.5 mg/mL, the S-phase fraction reached 34% at 24 hours and 44% at 48 hours in MDA-MB-231 cells.
AKT inhibitor comparator dose: 10 uM. Both LY294002 and AKT inhibitor III were used at this dose for the VEGF and conditioned-media capillary-morphogenesis lane.
How the study worked
Study design: The paper first ran dose- and time-response proliferation and viability assays in highly invasive MDA-MB-231 and less invasive MCF-7 breast-cancer cells using 0 to 1.0 mg/mL extract for 24, 48, and 72 hours. It then followed the invasive MDA-MB-231 line into 14-day soft-agar colony formation, 24- to 48-hour S-phase cell-cycle analysis at 0.5 mg/mL, western blots for p27 and AKT phosphorylation, vitronectin adhesion, Transwell migration, Matrigel invasion, uPA secretion, direct HAEC capillary morphogenesis, conditioned-media capillary morphogenesis, VEGF ELISA, and a pharmacologic AKT-comparator lane using LY294002 and AKT inhibitor III at 10 uM.. The study operates entirely in cell culture. MDA-MB-231 is the main disease model for invasion, uPA, VEGF, p27, and AKT analyses, while MCF-7 is used as a lower-invasiveness proliferation comparison. Human aortic endothelial cells were used on Matrigel for direct and conditioned-media capillary-morphogenesis assays. The paper also mentions prostate cell findings not shown, but the public page should stay on the breast-cancer and HAEC intervention evidence that is actually presented. Intervention: The intervention was a commercial aqueous Phellinus linteus extract given to breast-cancer or endothelial cells from 0 to 1.0 mg/mL, with most mechanistic emphasis on MDA-MB-231 cells and a lower 0 to 0.5 mg/mL range for the HAEC angiogenesis lane.. Comparator: Untreated cells are the main comparator, but the paper also compares less invasive MCF-7 against MDA-MB-231 growth sensitivity, direct PL exposure against PL-conditioned media in HAECs, and PL against two pharmacologic AKT inhibitors for the VEGF and capillary-morphogenesis lane.. Dose: Most cancer-cell assays used 0 to 1.0 mg/mL extract, while the endothelial and VEGF lanes used 0 to 0.5 mg/mL. LY294002 and AKT inhibitor III were each used at 10 uM.. Duration: Growth and viability were followed over 24 to 72 hours, colony formation over 14 days, migration over 5 hours after a 1-hour pretreatment, invasion over either 48 hours in the results text or 72 hours in the methods text, and HAEC morphogenesis over 16 hours..
Main outcomes included breast-cancer cell proliferation and colony formation, adhesion, migration, invasion, and uPA secretion in MDA-MB-231 cells, direct and conditioned-media HAEC capillary morphogenesis with VEGF secretion and AKT phosphorylation support, cell viability versus cytostatic interpretation, S-phase distribution and p27 expression in MDA-MB-231 cells, LY294002 and AKT inhibitor III comparator effects on VEGF and HAEC morphogenesis. Analysis population: Triplicate and repeated in-vitro assays across MDA-MB-231, MCF-7, and HAEC systems, with the invasive MDA-MB-231 line carrying most of the mechanistic weight.. Dropouts: Not reported. The paper does not describe excluded wells, failed blots, or omitted morphogenesis fields.. The biggest technical caveats are the undefined extract chemistry, the unresolved conditioned-media confound in the HAEC assays, and the internal inconsistency in invasion-assay timing.
Who was studied
MDA-MB-231 invasive breast-cancer cells as the main intervention model, MCF-7 breast-cancer cells as a sensitivity comparison, and HAEC endothelial tube-formation assays for the angiogenesis lane.
What this study cannot tell us
The intervention is a commercial aqueous extract without chemical fingerprinting, purified active fraction, or batch-standardization data.
The paper never tests breast-cancer tumors in animals or humans, so every claim lives inside cell-culture models.
Many of the anti-invasive and angiogenesis readouts are presented as figure-based dose responses without a compact text table of exact endpoint values.
The conditioned-media angiogenesis lane is partly confounded because the authors state that PL could not be removed from the conditioned media, so the HAEC effect is both direct and indirect.
The invasion assay timing is internally inconsistent across the paper: methods say 72 hours, the results text says 48 hours, and the figure caption says 24 hours.
How to read the evidence
The paper is useful because several invasion and angiogenesis-related phenotypes move together, but the undefined extract and missing in-vivo breast-cancer follow-through keep the claim boundary narrow.
When this study was published
Published 18 years ago in 2008. Older studies can still matter, but age increases the importance of later replication and updated methods.
The bigger picture
2003: Phellinus anti-angiogenic activity had already been reported before the breast-cancer mechanism paper An earlier 2003 Phellinus page in this database framed the species as anti-angiogenic in broader extract work. The current paper narrows that claim into a cancer-cell and endothelial-cell VEGF context.
2005: The same lab had already linked another mushroom extract to VEGF-suppression-driven angiogenesis control A 2005 Ganoderma paper from the same Sliva-Harvey line used a similar cancer-cell-secreted-VEGF and endothelial-morphogenesis logic, which makes the present study look like a breast-cancer extension of an existing assay frame rather than a brand-new concept.
2006: Phellinus metastasis work had already reached adhesion and invasion in another cancer model A 2006 Phellinus acidic-polysaccharide paper in this database linked the mushroom to melanoma metastasis control through adhesion and invasion blocking. The present study carries that phenotype into invasive breast-cancer cells and adds uPA, VEGF, and AKT detail.
2008: This paper consolidated growth, invasion, angiogenesis, and AKT into one breast-cancer extract story Sliva and colleagues pulled together cytostatic growth arrest, anti-invasive behavior, lower uPA, lower VEGF, lower p-AKT, and endothelial tube-formation suppression in one breast-cancer-focused extract paper.
2010: Later Phellinus work moved from pure cell culture into a mouse-supported prostate-cancer lane A later 2010 Phellinus extract study in this database pushed the species into athymic nude mice with advanced prostate cancer cells. That matters here because it shows the field trying to leave the cell-only zone that still limits the current paper.
Replication
2003: Phellinus anti-angiogenic activity had already been reported before the breast-cancer mechanism paper 2005: The same lab had already linked another mushroom extract to VEGF-suppression-driven angiogenesis control 2006: Phellinus metastasis work had already reached adhesion and invasion in another cancer model 2008: This paper consolidated growth, invasion, angiogenesis, and AKT into one breast-cancer extract story 2010: Later Phellinus work moved from pure cell culture into a mouse-supported prostate-cancer lane
Funding
The acknowledgments state that the work was supported by the Methodist Health Foundation, the Department of the Army Medical Research and Materiel Command Breast Cancer Research Training Program, and Maitake Products Inc.
Conflicts of interest
The article did not publish a formal conflict-of-interest statement. The extract was supplied by Maitake Products Inc., which is also listed in the acknowledgments as a funder.
Questions still open
- Do these laboratory findings hold up in animal or human studies?
- Do the observed effects persist beyond growth and viability were followed over 24 to 72 hours, colony formation over 14 days, migration over 5 hours after a 1-hour pretreatment, invasion over either 48 hours in the results text or 72 hours in the methods text, and haec morphogenesis over 16 hours.?
- This paper supports that an aqueous Phellinus linteus extract suppressed multiple malignant phenotypes in cultured breast-cancer cells and reduced HAEC capillary morphogenesis, with lower uPA, lower VEGF, and lower AKT phosphorylation moving in the same direction?
Common questions
What did this this mushroom topic study actually test?
What is the biggest reason not to overstate this paper?
What question does this study leave unanswered?
Read the original research
Phellinus linteus suppresses growth, angiogenesis and invasive behaviour of breast cancer cells through the inhibition of AKT signalling.
British journal of cancer, 98(8), 1348-56
Open-access 2008 breast-cancer cell paper testing a commercial aqueous Phellinus linteus extract across proliferation, invasion, endothelial morphogenesis, VEGF, uPA, and AKT readouts.
Citation
Sliva, D; Jedinak, A; Kawasaki, J; Harvey, K; Slivova, V. (2008). Phellinus linteus suppresses growth, angiogenesis and invasive behaviour of breast cancer cells through the inhibition of AKT signalling.. British journal of cancer, 98(8), 1348-56. https://doi.org/10.1038/sj.bjc.6604319