Selfheal (Prunella vulgaris) and Cancer (anticancer research): evidence and sources

To investigate and systematically describe the mechanism of action of() against digestive system tumors and related toxicity reduction. This study briefly describes the history of medicinal food and the pharmacological effects of, focusing on the review of the anti-digestive tumor effects of the active ingredients ofand the mechanism of its toxicity reduction. The active ingredients ofmay exert anti-tumor effects by inducing the apoptosis of cancer cells, inhibiting angiogenesis, inhibiting the migration and invasion of tumor cells, and inhibiting autophagy. In addition,active ingredients inhibit the release of inflammatory factors and macrophages and increase the level of indicators of oxidative stress through the modulation of target genes in the pathway to achieve the effect of toxicity reduction. The active ingredients in the medicine food homology plantnot only treat digestive system tumors through different mechanisms but also reduce the toxic effects.is worthy of being explored more deeply.

Triple-negative breast cancer (TNBC) is a type of breast cancer characterized by high molecular heterogeneity. Owing to the lack of effective therapeutic strategies, patients with TNBC have a poor prognosis.L. has the effects of reducing swelling, dissolving knots and treating breast carbuncles and mammary rocks. Modern pharmacological studies have reported that it can effectively inhibit the growth of breast cancer. The main active antitumor components ofare triterpenoids (PVT); however, the role and potential mechanism of PVT in TNBC remain unexplored. Our study aimed to further explore the inhibitory effects of PVT on TNBC and the associated mechanism. The results showed that 19 compounds associated with PVT were identified, 9 of which were triterpenoids. The percentages of ursolic acid and oleanolic acid in PVT were 34.51% and 11.32%, respectively. Triterpenes ofsignificantly inhibited the proliferation, migration and invasion of MDA-MB-231 cells and promoted their apoptosis in a concentration-dependent manner. PVT could also effectively downregulate the mRNA and protein expression levels of,,andand upregulate the mRNA and protein expression levels ofin MDA-MB-231 cells. In mice with tumors of TNBC, PVT significantly reduced tumor growth and the expression levels of PTP1B, CXCL12, CXCR4, PI3K, AKT, mTOR and other proteins in TNBC tumor tissue and upregulated the expression of IL-24. This study showed that PVT played an anti-TNBC role by regulating the PTP1B/PI3K/AKT/mTOR signaling pathway and the IL-24/CXCL12/CXCR4 signaling axis.

Lymph node metastasis (LNM) in papillary thyroid carcinoma (PTC) is a major contributor to poor prognosis. Prunella vulgaris (P. vulgaris), a traditional medicinal herb, has shown potential in inhibiting PTC metastasis, but its molecular mechanism remains unclear. This study aimed to elucidate the molecular mechanisms by which P. vulgaris exerts its anti-metastatic effects on PTC, focusing on identifying key active compounds and their target genes. RNA sequencing was used to identify differentially expressed genes (DEGs) between PTC and LNM tissues. Active compounds and targets of P. vulgaris were obtained from TCMSP and BATMAN-TCM and integrated with DEGs to construct a compound-target network. Machine-learning algorithms were applied to identify hub genes related to β-sitosterol (BS). The effects of BS and ADRB2 on cell viability, proliferation, migration, invasion, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) were examined in vitro. 696 DEGs and 195 P vulgaris targets were identified, with 91 overlapping genes intersecting DEGs and P. vulgaris targets. Within this network, 17 target genes were associated with BS, and five machine-learning algorithms consistently identified ADRB2 as a central hub. ADRB2 expression was significantly elevated in LNM tissues and closely correlated with clinicopathological features. BS treatment inhibited PTC cell growth and metastasis-related behaviors, which were reversed by ADRB2 overexpression. BS, an active component of P. vulgaris, inhibits key processes associated with PTC metastasis by targeting ADRB2 and inducing mitochondrial dysfunction. These findings not only provide the first experimental evidence linking BS to ADRB2-mediated anti-metastatic activity in PTC, but also offer a novel integrated approach for identifying therapeutic compounds from traditional herbs.

Prunella vulgaris (PV) is widely used in treating various diseases, but its relationship with hepatocellular carcinoma (HCC) remains unclear. This study systematically evaluates PV's therapeutic potential in HCC and explores its molecular mechanisms. Active compounds and molecular targets of PV were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database, and HCC-related targets were identified using the Gene Expression Omnibus database. A drug-disease target network was built to identify key hub genes, which were further investigated through immune analysis, single-cell RNA sequencing, molecular docking, and in vitro experiments. We identified 185 drug targets and 635 HCC-related targets, with 15 potential PV targets linked to HCC progression. In vitro validation confirmed significant expression of these targets in HCC cells. Mechanistic analysis indicated that these hub genes may influence HCC progression through pathways like tumor protein 53 signaling and are associated with immune cell subsets, including CD8+ T cells and natural killer cells. This study identifies key bioactive components of PV for HCC treatment and reveals their molecular mechanisms. Dysregulation of these targets correlates with HCC pathogenesis, suggesting their potential as novel biomarkers. Future research will focus on further validation in vitro and in vivo to explore the clinical applicability of these targets and the synergistic potential of PV in combination with other treatments.

The herbhas shown significant immune-stimulatory and anti-inflammatory effects in mouse models. Here, the effects of a novel-containing herbal mixture, PV-1, were examined in several mouse models for cancer, including chemically induced models of lung and oral cancers as well as syngraft models for lung cancer and melanoma. PV-1, consisting of extracts from,,and, exhibited no toxicity in a dose escalation study in A/J mice. PV-1 significantly inhibited mouse lung tumor development induced by the lung carcinogens vinyl carbamate and benzo[a]pyrene. PV-1 also hindered the induction of oral squamous cell carcinomas in C57BL/6 mice caused by 4-nitroquinoline-1-oxide. Flow cytometry analysis showed that PV-1 increased the numbers of CD8+ tumor-infiltrating lymphocytes (TILs) and increased the production of granzyme B, TNF-α, and IFN-γ by CD8+ TILs. PV-1 also suppressed granulocytic myeloid-derived suppressor cell numbers (g-MDSCs) and improved the anti-cancer activity of anti-PD-1 immunotherapy. These results indicate that PV-1 remodels the tumor immune microenvironment by selectively inhibiting g-MDSCs and increasing CD8+ TILs within tumors, resulting in decreased immune suppression and enhanced cancer chemopreventive efficacy.

extract (PVE) was shown to promote apoptosis in differentiated thyroid cancer (DTC) cells. However, whether other mechanisms are involved in the antitumour effect of PVE in thyroid cancer (TC) cells remains unclear. The present study aimed to investigate the antiproliferative and antimigratory effects of PVE on TC cell lines both in vitro and in vivo. First, the TPC-1 and SW579 human TC cell lines were screened by MTT assay for their high level of sensitivity to PVE. Then, the results of cell growth curve and colony formation assay and cell cycle analyses, wound healing, and migration assays demonstrated that PVE inhibited the proliferation and migration of TPC-1 and SW579 cells. Moreover, the antitumour effect of PVE was verified in a subcutaneous xenotransplanted tumour model. Next, MKI67, PCNA, CTNNB1, and CDH1 were screened by qRT-PCR for their significantly differential expression levels in xenograft tissue with and without PVE treatment, and expression of MKI67, PCNA, and CDH1 was verified by Western blot. Finally, an integrated bioinformatics analysis containing protein-protein interaction network, KEGG pathway, and GO analysis was conducted to explore more potential antitumour mechanisms of PVE. In summary, PVE could inhibit the proliferation and migration of TC cells both in vitro and in vivo, which may have been achieved by modulation of the expression of MKI67, PCNA, and CDH1. These data suggest that PVE has the potential to be developed into a new anticancer drug for the treatment of TC.

BACKGROUND: The flowers and dried fruit spikes of Prunella vulgaris L. (P. vulgaris L.) have been widely used in traditional Chinese medicine and food. P. vulgaris L. is regarded as a good option for treating uterine myoma (UM). However, scientific evidence of anti-UM activity of the extract of P. vulgaris L. (PVE) is lacking. The present study aimed to characterize the chemical composition of PVE and evaluate the pharmacodynamics and mechanism of PVE against UM. METHODS: The chemical composition of PVE was analyzed by GC-MS. MTT was used to screen and evaluate cell proliferation and toxicity. Double fluorescence flow cytometry method were used to determine the apoptosis and cell cycle progression of UM cells under PVE treatment. The anti-UM activity of PVE was investigated by using a specific-pathogen-free (SPF) rat model of UM. TUNEL staining was used to detect the apoptosis of UM cells. The concentrations of estrogen and progesterone in the serum of SPF rats were detected by ELISA. The expression levels of PCNA, estrogen receptor alpha, estrogen receptor beta, progesterone receptor, survivin, caspase-3, Bax and Bcl-2 in the uterus of SPF rats was detected by immunohistochemistry (IHC). RESULTS: The extraction rate of PVE was 8.1%. The main components were squalene (28.3%), linoleic acid (9.96%), linolenic acid (9.95%), stearic acid (6.26%) and oleic acid (5.51%). In vitro, PVE had significant anti-human UM cell activity, exhibited no drug toxicity, promoted the apoptosis of human UM cells, and inhibited the transition of UM cells from the G0/G1 stage into the G2 stage, in which DNA replication occurs. In vivo, PVE had significant anti-UM activity. PVE decreased the concentrations of estrogen and progesterone and downregulated the expression levels of the estrogen and progesterone receptors through the estrogen signaling pathway. PVE also promoted the apoptosis of UM cells by downregulating the expression levels of the survivin and Bcl-2 proteins and upregulating the expression levels of caspase-3 and Bax through the mitochondria-mediated apoptotic pathway. CONCLUSION: PVE has marked anti-UM activity. PVE can be used as an ideal candidate drug to treat UM.

Metastasis is the main cause of cancer-related deaths. Anoikis is a type of apoptosis caused by cell detachment, and cancer cells become anoikis resistant such that they survive during circulation and can successfully metastasize. Therefore, sensitization of cancer cells to anoikis could prevent metastasis. Here, by screening for anoikis sensitizer using natural compounds, we found that pygenic acid A (PA), a natural compound from Prunella vulgaris, not only induced apoptosis but also sensitized the metastatic triple-negative breast cancer cell lines, MDA-MB-231 cells (human) and 4T1 cells (mouse), to anoikis. Apoptosis protein array and immunoblotting analysis revealed that PA downregulated the pro-survival proteins, including cIAP1, cIAP2, and survivin, leading to cell death of both attached and suspended cells. Interestingly, PA decreased the levels of proteins associated with anoikis resistance, including p21, cyclin D1, p-STAT3, and HO-1. Ectopic expression of active STAT3 attenuated PA-induced anoikis sensitivity. Although PA activated ER stress and autophagy, as determined by increases in the levels of characteristic markers, such as IRE1α, p-elF2α, LC3B I, and LC3B II, PA treatment resulted in p62 accumulation, which could be due to PA-induced defects in autophagy flux. PA also decreased metastatic characteristics, such as cell invasion, migration, wound closure, and 3D growth. Finally, lung metastasis of luciferase-labeled 4T1 cells decreased following PA treatment in a syngeneic mouse model when compared with the control. These data suggest that PA sensitizes metastatic breast cancer cells to anoikis via multiple pathways, such as inhibition of pro-survival pathways and activation of ER stress and autophagy, leading to the inhibition of metastasis. These findings suggest that sensitization to anoikis by PA could be used as a new therapeutic strategy to control the metastasis of breast cancer.