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1.
Med Oncol ; 40(6): 179, 2023 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-37188900

RESUMO

Apelin/APJ axis plays a critical role in cancer progression, thus its targeting inhibits tumor growth. However, blocking of Apelin/APJ axis in combination with immunotherapeutic approaches may be more effective. This study aimed to investigate the effects of APJ antagonist ML221 in combination with a DC vaccine on angiogenic, metastatic and apoptotic-related factors in a breast cancer (BC) model. Four groups of female BALB/c mice with 4T1-induced BC were treated with PBS, APJ antagonist ML221, DC vaccine, and "ML221 + DC vaccine". After completion of the treatment, the mice were sacrificed and the serum levels of IL-9 and IL-35 as well as the mRNA expression of angiogenesis (including VEGF, FGF-2, and TGF-ß), metastasis (including MMP-2, MMP-9, CXCR4) and apoptosis-related markers (Bcl-2, Bax, Caspase-3) in tumor tissues were determined using ELISA and real-time PCR, respectively. Angiogenesis was also evaluated by co-immunostaining of tumor tissues with CD31 and DAPI. Primary tumor metastasis to the liver was analyzed using hematoxylin-eosin staining. The efficiency of combination therapy with "ML221 + DC vaccine" was remarkably higher than single therapies in preventing liver metastasis compared to the control group. In comparison with the control group, combination therapy could significantly reduce the expression of MMP-2, MMP-9, CXCR4, VEGF, FGF-2, and TGF-ß in tumor tissues (P < 0.05). It also decreased the serum level of IL-9 and IL-35 compared with the control group (P < 0.0001). Moreover, vascular density and vessel diameter were significantly reduced in the combination therapy group compared with the control group (P < 0.0001). Overall, our findings demonstrate that combination therapy using a blocker of the apelin/APJ axis and DC vaccine can be considered a promising therapeutic program in cancers.


Assuntos
Neoplasias da Mama , Neoplasias Hepáticas , Animais , Feminino , Camundongos , Apelina/genética , Apelina/metabolismo , Receptores de Apelina/genética , Receptores de Apelina/metabolismo , Neoplasias da Mama/terapia , Células Dendríticas/metabolismo , Fator 2 de Crescimento de Fibroblastos , Interleucina-9 , Metaloproteinase 2 da Matriz , Metaloproteinase 9 da Matriz , Fator de Crescimento Transformador beta , Eficácia de Vacinas , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo
2.
Iran J Microbiol ; 14(6): 874-880, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36721439

RESUMO

Background and Objectives: Few studies have considered potential benefits of probiotic bacteria and their derivatives on human and animal health. Nisin is an antimicrobial agent that is produced by lactobacilli and served as a preservative in foods. This study aims to investigate whether nisin suppresses or decreases the genes involved in the pathogenicity of methicillin-susceptible and methicillin-resistant Staphylococcus aureus (MSSA and MRSA). Materials and Methods: MSSA and MRSA strains were cultured at the », ½, and 1 × minimum inhibitory concentration (MIC) of nisin. Next, RNA extraction was performed at the mid-exponential stage of growth, and cDNA was synthesized. The expression of virulence factors was measured by qPCR, and the data were analyzed by the ΔΔCt formula. Results: Depending on the incubation times and the Lactobacillus species, the MIC of nisin on MRSA and MSSA observed in 800 and 1600 mg/l, respectively. The qPCR assay showed the expression level of the sea, agrA, and spa genes decreased and the level of the sae gene increased at the sub-MIC of nisin, and no antagonism was observed. Concerning MRSA, the maximum downregulation rate was observed in the sea gene (up to 5.9 folds) while in MSSA, the maximum downregulation rate was noticed in the agrA gene (up to 10 folds). Conclusion: Due to the high inhibitory effect of the sub-MIC of nisin on the expression of virulence factor genes in MRSA and MSSA, this compound could potentially reduce the virulence of S. aureus.

3.
Asian Pac J Cancer Prev ; 20(5): 1457-1462, 2019 May 25.
Artigo em Inglês | MEDLINE | ID: mdl-31127908

RESUMO

Objectives: Hepatocellular carcinoma is one of the most frequent cancers worldwide, for the treatment of which various therapy protocols and drugs have been introduced; however, none of them has suppressed cancer tissues completely. New research programs have been developed on cancer and the accompanied effects of novel synthesized compounds on cancer cell lines. Our latest reports on the molecular basis of cancer revealed a pattern of changes in gene expression triggered in the cancer pathway. Methods: HepG2 cell lines were cultured under similar conditions in both test and control groups. The IC50 concentration of the (2R, 4S)-N-(2, 5-difluorophenyl)-4-hydroxy-1-(2, 2, 2-trifluoroacetyl) pyrrolidine-2-carboxamide compound was used in the treatment group. After 48 hours from the culture, the expressional profiles of apoptosis pathway genes (84 genes) were studied using the PCR array method. Results: The findings demonstrated that the expression of some apoptosis-related genes pertaining to TNF, BCL2, IAP, and caspase families was regulated by (2R, 4S)-N-(2, 5-difluorophenyl)-4-Hydroxy-1-(2, 2, 2-Trifluoroacetyl) Pyrrolidine-2-Carboxamide. In the same vein, an alteration was observed in the expression of both pro-apoptotic and anti-apoptotic genes associated with the extrinsic and intrinsic apoptosis signaling pathways. Conclusions: According to the data obtained, the pyrrolidine-2-carboxamide compound was demonstrated to be able to regulate the apoptotic activities of HepG2 cells by affecting both pro-apoptotic and anti-apoptotic relevant genes.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Pirrolidinas/farmacologia , Proteínas Reguladoras de Apoptose/metabolismo , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/metabolismo , Caspases/metabolismo , Linhagem Celular Tumoral , Células Hep G2 , Humanos , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fatores de Necrose Tumoral/metabolismo
4.
J Cell Physiol ; 233(12): 9247-9260, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30076727

RESUMO

The eradication of cancer in a patient remains an elusive challenge despite advances in early detection and diagnosis, chemo- and immunotherapy, pinpoint radiation treatments, and expert surgical intervention. Although significant gains have been made in our understanding of cancer cell biology, a definite cure for most cancers does not exist at present. Thus, it is not surprising that the research and medical communities continue to explore the importance and therapeutic potential of natural products in their multimodality cancer treatment approach. Curcuminoids found in turmeric are one such class of natural products that have been extensively investigated for their potential to halt the progression of cancer cell proliferation and, more important, to stop metastasis from occurring. In this review, we examine one curcuminoid (demethoxycurcumin [DMC]) largely because of its increased stability and better aqueous solubility at physiological pH, unlike the more well-known curcuminoid (curcumin), which is largely unabsorbed after oral ingestion. The present review will focus on the signaling pathways that DMC utilizes to modulate the growth, invasion, and metastasis of cancer cells in an effort to provide enhanced mechanistic insight into DMC's action as it pertains to brain, ovarian, breast, lung, skin, and prostate cancer. Additionally, this review will attempt to provide an overview of DMC's mechanism of action by modulating apoptosis, cell cycle, angiogenesis, metastasis, and chemosensitivity. Lastly, it is hoped that increased understanding will be gained concerning DMC's interactive role with microRNA-551a, 5' adenosine monophosphate-activated protein kinase, nuclear factor-κB, Wnt inhibitory factor-1, and heat shock protein 70 to affect the progression of cancer.


Assuntos
Proliferação de Células/efeitos dos fármacos , Curcumina/análogos & derivados , Curcumina/uso terapêutico , Neoplasias/tratamento farmacológico , Proteínas Quinases Ativadas por AMP/genética , Apoptose/efeitos dos fármacos , Curcumina/química , Diarileptanoides , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , NF-kappa B/genética , Neoplasias/patologia , Transdução de Sinais/efeitos dos fármacos
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