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Oral squamous cell carcinoma (OSCC) is an aggressive malignancy characterized by high invasiveness and poor prognosis. This study investigated the anticancer mechanisms of eupatilin, a pharmacologically active flavonoid derived from species, in human OSCC YD-10B cells. Eupatilin significantly reduced cell viability in a dose-dependent manner, with an IC of approximately 50 μM. Flow cytometric analysis revealed G0/G1 phase arrest accompanied by downregulation of Cyclin D1 and CDK2, and upregulation of p21. Annexin V/Propidium Iodide staining and Western blotting confirmed apoptosis induction through activation of Bax, cleaved caspase-3/9, and poly ADP-ribose polymerase (PARP) cleavage, alongside suppression of Bcl-2. Furthermore, eupatilin markedly decreased both the mRNA expression and enzymatic activities of matrix metalloproteinases (MMP)-2 and MMP-9, indicating its potential to inhibit cancer cell invasion. Collectively, these findings demonstrate that eupatilin exerts potent antiproliferative and anti-invasive effects on OSCC cells via cell-cycle modulation and mitochondrial-mediated apoptosis. This study provides the first evidence of eupatilin's therapeutic potential against OSCC, suggesting its promise as a natural compound for the development of safer and more effective treatments for oral cancer.

Prostate cancer is one of the most common cancers in men. Cell invasion is an important step in the process of cancer metastasis. Herein, gold nanorods (GNRs) and polyethylene glycol (PEG)-coated GNRs were conjugated with polydopamine (PDA). The PDA-nanoconjugates demonstrated excellent colloidal stability upon lyophilization and dispersion in cell culture media with or without the addition of fetal bovine albumin (FBS), compared to unconjugated GNRs. PDA-nanoconjugates exhibited a considerable cytotoxicity against DU-145 and PC3 prostate cancer cell lines over a concentration range of 48 μg/mL–12 μg/mL, while they were biocompatible over a concentration range of 3.0 μg/mL–0.185 μg/mL. Furthermore, PDA-nanoconjugates demonstrated possible anti-invasion activity towards prostate cancer cell lines, particularly DU-145 cell line, by reducing cell migration and cell adhesion properties. The PDA-nanoconjugates could be considered a promising nano-platform toward cancer treatment by reducing the invasion activity; it could also be considered a drug delivery system for chemotherapeutic agents.

Ginsenoside Rg3, a naturally occurring phytochemical, serves an important role in the prevention and treatment of cancer. In the present study, with the aim to reveal the molecular mechanism of Rg3 in liver cancer cell metastasis, the anti-migration and anti-invasion effects of Rg3 on liver cancer cells were investigated. It was demonstrated that Rg3 caused marked inhibition of cell migration and invasion of human liver cancer cells, HepG2 and MHCC-97L, in vitro, and the growth of HepG2 and MHCC-97L tumors in BABL/c nude mice. The protein expression of Rho GTPase activating protein 9 (ARHGAP9) was increased both in HepG2 and MHCC-97L cells. Following ARHGAP9 knockdown, the results of Transwell and tumorigenesis assays revealed that the anti-migration, anti-invasion and anti-tumor growth effects of Rg3 were impaired significantly. The increased expression of ARHGAP9 protein induced by Rg3 was remarkably suppressed. All results suggested that ARHGAP9 protein may be a vital regulator in the anti-metastatic role of Rg3. To the best of our knowledge, the present study is the first to report that Rg3 effectively suppressed the migration and invasion of liver cancer cells by upregulating the protein expression of ARHGAP9, indicating a novel natural therapeutic agent and a therapeutic target for the treatment of liver cancer.

Background: Cynanchum paniculatum (Bunge) Kitag. ex H.Hara, a member of the Asclepiadaceae family, has a rich history as a traditional Chinese medicinal plant used to treat digestive disorders. However, its potential anti-cancer effects in pancreatic cancer remain largely unexplored. Aim: This study delves into the intricate anti-pancreatic cancer mechanisms of C. paniculatum (Bunge) Kitag. ex H.Hara aqueous extract (CPAE) by elucidating its role in apoptosis induction and the inhibition of invasion and migration. Methods: A comprehensive set of methodologies was employed to assess CPAE’s impact, including cell viability analyses using MTT and colony formation assays, flow cytometry for cell cycle distribution and apoptosis assessment, scratch-wound and Matrigel invasion assays for migration and invasion capabilities, and immunoblotting to measure the expression levels of key proteins involved in apoptosis and metastasis. Additionally, a murine xenograft model was established to investigate CPAE’s in vivo anti-cancer potential. Results: CPAE exhibited time- and dose-dependent suppression of proliferation and colony formation in pancreatic cancer cells. Notably, CPAE induced apoptosis and G2/M phase arrest, effectively activating the caspase-dependent PARP pathway. At non-cytotoxic doses, CPAE significantly curtailed the metastatic abilities of pancreatic cells, effectively suppressing epithelial-mesenchymal transition (EMT) and downregulating the TGF-β1/Smad2/3 pathway. In vivo experiments underscored CPAE’s ability to inhibit tumor proliferation. Conclusion: This study illuminates the multifaceted anti-proliferative, pro-apoptotic, anti-invasive, and anti-migratory effects of CPAE, both in vitro and in vivo . CPAE emerges as a promising herbal medicine for pancreatic cancer treatment, with its potential mediated through apoptosis induction via the caspase-dependent PARP pathway and MET suppression via the TGF-β1/Smad2/3 signaling pathway at non-cytotoxic doses. These findings advocate for further exploration of CPAE’s therapeutic potential in pancreatic cancer.

KT2 is a lysine/tryptophan-rich peptide modified from Crocodylus siamensis Leucrocin I. In this study, we examined the cell toxicity, cellular uptake, anti-migration and anti-invasion activities of KT2 in A375.S2 human melanoma cells. A375.S2 cells were treated with KT2 peptide and then we performed MTT assay, study of cellular uptake by a confocal microscope, wound healing assay, transwell migration/invasion assay, and evaluation of the expression of metastasis-associated proteins. KT2 can be internalized through the plasma membrane and can slightly alter cell morphology, decrease the percentage of viable cells and inhibit cell migration and invasion of A375.S2 cells in a dose-dependent manner. This peptide suppressed MMP-2 activity, as measured by gelatine zymography assay. The protein level of MMP-2 was decreased by KT2. KT2 also down-regulated metastasis pathway-related molecules, including FAK, RhoA, ROCK1, GRB2, SOS-1, p-JNK, p-c-Jun, PI3K, p-AKT (Thr308), p-AKT (Ser473), p-p38, MMP-9, NF-kB, and uPA. These results indicate that KT2 inhibits the migration and invasion of human melanoma cells by decreasing MMP-2 and MMP-9 expression through inhibition of FAK, uPA, MAPK, PI3K/AKT NF-kB, and RhoA-ROCK signalling pathways. These findings suggest that KT2 deserves further investigation as an anti-metastatic agent for human melanoma.

Chemotherapy is a palliative treatment for unresectable patients with cholangiocarcinoma (CCA). However, drug resistance is a major cause of the failure of this treatment. Derrischalcone (DC), a novel chalcone isolated from Derris indica fruit, has been shown pharmacologically active; though, the effect of DC on CCA is unknown. The present study investigated the cytotoxic, antiproliferative, anti-migration, and anti-invasion effects and underlying mechanisms of DC on CCA KKU-M156 and KKU-100 cells. Cytotoxicity and apoptosis were evaluated by acridine orange and ethidium bromide fluorescent staining. Reactive oxygen species (ROS) was measured by dihydroethidium assay. Cell proliferation and reproductive cell death were assessed by sulforhodamine B staining and colony-forming assay. Migration and invasion were determined by wound healing and transwell chamber assays. Protein expressions associated with cell death, proliferation, migration, and invasion were analyzed by western immunoblotting. We found that DC induced cytotoxicity and apoptosis in association with ROS formation and oxidative stress. Treatment with N -acetylcysteine suppressed ROS formation and attenuated DC-induced cytotoxic and apoptotic effects. DC increased the expression of p53, p21, Bax, and cytochrome c proteins in association with cell death. DC-induced antiproliferation, colony formation, anti-migration, and anti-invasion were associated with the suppression of Akt/mTOR/cyclin D1 and FAK signaling pathways. These findings suggest that the multi-targeting strategies with DC may be a novel treatment for cancer therapy.

( ) is a major foodborne pathogen which can invade intestinal epithelial cells and cause severe systemic infection. Probiotics, as well as their surface layer proteins, hold broad promise for enhancing intestinal barrier function and defending against pathogenic invasion. In the present study, the antagonistic effects of surface layer protein ornithine carbamoyltransferase (OTC) from ( ) WEFA23 against were systematically evaluated in vitro in human intestinal epithelial Caco-2 cells, including assessments of anti-adhesion and anti-invasion capacity, inflammatory cytokine responses, intestinal barrier integrity, and transcriptomic changes, by comparing the effects of wild-type WEFA23 and a previously constructed WEFA23 gene knockout strain ( WEFA23 ). The results demonstrated that WEFA23 achieved significant stronger anti-adhesion and anti-invasion capacity of ( < 0.05) in the presence of OTC, potentially through increasing tight junction protein expression, regulating inflammatory cytokines, and modulating the virulence factors of the pathogen. To elucidate the potential mechanism of the inhibitory effect of OTC protein, RNA-seq was performed. The results revealed that the significantly regulated core differentially expressed genes (DEGs), including , , , and , were found to be involved in γ-aminobutyric acid (GABA)-ergic synapse, calcium, and toll-like receptor signaling pathways. These findings demonstrated that OTC is involved in blocking invasion and revealed the function of the OTC from WEFA23 in antimicrobial and intestinal mucosal defense, providing a conceptual foundation for the development of new probiotic intervention strategies in anti-infection.

Elephantopus mollis Kunth H.B et Kunth is an herbal plant employed customarily for the treatment of numerous maladies, notably cancers. Here in this research, we studied the effects of E. mollis ( EM ) petroleum ether extract (EM-PE) on the highly aggressive breast cancer cell line MDA-MB-231. The result from phytochemical analysis demonstrated the presence of tannins and saponins in EM-PE, of which, saponins made up more than 50% of the extract’s mass. Cytotoxicity results, which were obtained from MTT assay and microscopic observation, suggested the potential of EM-PE to inhibit the growth of MDA-MB-231 cells with low IC 50 value (approximately 30 μg/mL) and remarkably high selectivity index (> 4.78). Further evaluation indicated that EM-PE inhibited MDA-MB-231 cells growth in a dose-dependent manner. Interestingly, we found that EM-PE induced senescence in MDA-MB-231 cells via the activation of senescence-associated β-galactosidase and the transcriptional upregulation of p21 (3.7 times) and p27 (1.4 times). In consistent with this effect, pre-treated cancer cells showed no proliferative recovery after EM-PE removal. In addition, EM-PE could dramatically hinder breast cancer cells invasion (as much as 15.07-fold), which was shown in Transwell invasion assay, together with the decreased transcription of the important metastatic-involved SNAIL1 gene. Overall, our study, for the first time, exhibits the anti-proliferation and anti-invasion effects of EM extract on highly metastasis breast cancer cell line MDA-MB-231. Hence, these findings contributed to the knowledge of anti-cancer potential of this herbal plant .

Metastasis remains the leading cause of death among patients with non-small cell lung cancer (NSCLC), emphasizing the urgent need for safer and more effective therapeutic options. Mitogen-activated protein kinase (MAPK) pathways play a crucial role in regulating EMT, migration, and invasion in NSCLC. Targeting these molecular mechanisms has become a key strategy in inhibiting NSCLC metastasis. Loureirin A and Loureirin B, flavonoids derived from the Thai traditional herb Dracaena loureiri, have shown potential pharmacological effects; however, their roles in NSCLC metastasis remain unexplored. This study aimed to elucidate the mechanisms by which Loureirin A and Loureirin B suppress EMT, migration, and invasion in NSCLC cells via the MAPK signaling pathway. The sulforhodamine B (SRB) assay showed that Loureirin A and Loureirin B, at concentrations ranging from 0 to 140 μM, were non-toxic to both A549 and H1299 cells. Additionally, Loureirins A and B exhibited no cytotoxic effects on primary human dermal fibroblast cells and did not induce hemolysis in red blood cells (RBCs). The wound-healing and trans-well assays were used to evaluate the anti-migratory and anti-invasion properties of Loureirin A and Loureirin B in NSCLC cell lines. Gelatin zymography was employed to investigate the activity of MMP-2 (gelatinase A) and MMP-9 (gelatinase B), while Western blot analysis was used to examine the expression of EMT markers and invasive proteins, and the phosphorylation of MAPK signaling molecules. Our results demonstrate that both Loureirin A and Loureirin B significantly suppressed the migration and invasion of A549 and H1299 cells. These compounds suppressed the activity of matrix metalloproteinases MMP-2 and MMP-9 and downregulated the expression of key invasive proteins including uPA, uPAR, and MT1-MMP. Additionally, they effectively suppressed the expression of EMT markers such as N-cadherin, Vimentin, and Fibronectin. Mechanistically, Loureirin A and Loureirin B inhibited the MAPK signaling pathway by downregulating the phosphorylation of ERK, JNK, and p38 proteins. In conclusion, these findings demonstrate that Loureirin A and Loureirin B exhibit potent anti-invasive properties and no cytotoxic effect on NSCLC cell lines, suggesting their potential as promising candidates for anti-cancer drug development. Furthermore, they may pave the way for the exploration of combination therapies with other anti-cancer drugs for clinical translation.

Interferon-induced transmembrane protein 1 (IFITM1) has recently been identified as a new molecular marker in human colorectal cancer. However, its role in glioma carcinogenesis is not known. In this study, we demonstrated that suppression of IFITM1 expression significantly inhibited proliferation of glioma cells in a time-dependent manner. The growth inhibitory effect was mediated by cell cycle arrest. Furthermore, IFITM1 knockdown significantly inhibited migration and invasion of glioma cells, which could be attributed to decreased expression and enzymatic activity of matrix metalloproteinase 9. Taken together, these results suggest that IFITM1 is a potential therapeutic target for gliomas.