scholarly journals A novel taspine derivative suppresses human liver tumor growth and invasion in vitro and in vivo

2013 ◽  
Vol 6 (3) ◽  
pp. 855-859 ◽  
Author(s):  
NAN WANG ◽  
LEI ZHENG ◽  
YINGZHUAN ZHAN ◽  
YANMIN ZHANG
Keyword(s):  
Tumor Growth ◽  
Liver Tumor ◽  
Human Liver ◽  
Tumor Growth And Invasion

S100A3 Suppression Inhibits In Vitro and In Vivo Tumor Growth and Invasion of Human Castration-resistant Prostate Cancer Cells

Urology ◽  
2015 ◽  
Vol 85 (1) ◽  
pp. 273.e9-273.e15 ◽  
Author(s):  
Minyong Kang ◽  
Hye Sun Lee ◽  
Young Ju Lee ◽  
Woo Suk Choi ◽  
Yong Hyun Park ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Castration Resistant Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Castration Resistant ◽  
Tumor Growth And Invasion

scholarly journals Extracellular vesicles from human liver stem cells inhibit renal cancer stem cell‐derived tumor growth in vitro and in vivo

2020 ◽  
Vol 147 (6) ◽  
pp. 1694-1706 ◽  
Author(s):  
Alessia Brossa ◽  
Valentina Fonsato ◽  
Cristina Grange ◽  
Stefania Tritta ◽  
Marta Tapparo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Tumor Growth ◽  
Extracellular Vesicles ◽  
Renal Cancer ◽  
Human Liver ◽  
Liver Stem Cells

HMGB1 Derived from Macrophages Acts as an Angiogenic Factor.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3852-3852
Author(s):  
Ikuro Maruyama ◽  
Ko-ichi Kawahara ◽  
Takashi Ito ◽  
Yoko Oyama ◽  
Kazunori Takenouchi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Advanced Glycation Endproducts ◽  
High Mobility ◽  
Cellular Migration ◽  
Angiogenic Factor ◽  
Hmgb1 Protein ◽  
Glycation Endproducts ◽  
Tumor Growth And Invasion

Abstract High Mobility Group Box-1 (HMGB1) protein, released from the most of necrotic cells and activated macrophages, has been identified as a novel cytokine through the receptor for advanced glycation endproducts (RAGE) and Toll-like receptor(TLR)-2 and -4. The HMGB1-RAGE and TLRs-2, -4 interactions contribute to cellular migration and the production of proinflammatory cytokines, and participate in pathomechanisms in tumor growth and invasion, in which an angiogenesis development is an important aspect. We here show that HMGB1 stimulates the expression of Vascular Endothelial Growth Factor (VEGF), the most potent angiogenic factor in tumors, through the HMGB1-RAGE, but neither TLR-2 nor TLR-4 in macrophage-lineage cells in vitro. The mechanism of VEGF production is mediated through the Akt pathway, which is linked to tumor growth and invasion. Furthermore, HMGB1 induced angiogenesis was also observed in an in vivo rabbit corneal assay (Fig). These results suggest that HMGB1, released from the tumor-associated macrophages, may act as a key cytokine in the development of angiogenesis by producing VEGF in tumor growth and invasion. Thus the tumor-associated HMGB1/RAGE system may contribute to our understanding of the mechanism of cancer cell escape from macrophage-associated acceleration of inflammation.

Antitumor activity of Pulsatilla chinensis (Bunge) Regel saponins in human liver tumor 7402 cells in vitro and in vivo

Phytomedicine ◽  
2012 ◽  
Vol 19 (3-4) ◽  
pp. 293-300 ◽  
Author(s):  
Qiong-ming Xu ◽  
Zhan Shu ◽  
Wen-jun He ◽  
Lan-ying Chen ◽  
Shi-lin Yang ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Liver Tumor ◽  
Human Liver ◽  
Pulsatilla Chinensis

scholarly journals Small interfering RNA targeting CDC25B inhibits liver tumor growth in vitro and in vivo

2008 ◽  
Vol 7 (1) ◽  
pp. 19 ◽  
Author(s):  
Xinrui Yan ◽  
Mei-Sze Chua ◽  
Jing He ◽  
Samuel K So
Keyword(s):  
Tumor Growth ◽  
Liver Tumor ◽  
Small Interfering Rna ◽  
Rna Targeting ◽  
Interfering Rna

scholarly journals Expression and clinical significance of HMGB1 in human liver cancer: Knockdown inhibits tumor growth and metastasis in vitro and in vivo

2012 ◽  
Vol 29 (1) ◽  
pp. 87-94 ◽  
Author(s):  
YA-DONG DONG ◽  
LONG CUI ◽  
CHENG-HONG PENG ◽  
DONG-FENG CHENG ◽  
BAO-SAN HAN ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Clinical Significance ◽  
Human Liver ◽  
Human Liver Cancer ◽  
Tumor Growth And Metastasis

scholarly journals DPP3 Expression Promotes Cell Proliferation and Migration in Vitro and Tumor Growth in Vivo That Associates with Poor Prognosis of Esophageal Carcinoma

2021 ◽  
Author(s):  
Jing-Kun Liu ◽  
Abulizi Abudula ◽  
Hai-Tao Yang ◽  
Li-Xiu Xu ◽  
Ge Bai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Tumor Growth ◽  
Esophageal Carcinoma ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Esophageal Cancer Cells ◽  
Tumor Growth And Invasion

Abstract Background: Dipeptidyl peptidase III (DPP3) is a zinc-dependent metallopeptidase and elevated in a variety of malignant tumors, but the underlying mechanism is not well understood so far. Here we investigated the association of esophageal carcinogenesis with the regulation of DPP3 expression by tissue-based quantitative analysis and the depletion of DPP3 expression in esophageal cancer cells and xenograft model. Methods: The expression level of DPP3 in esophageal cancer tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with esophageal carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3-depleted esophageal cancer cells created by infection with the lentivirus containing the shRNA specific to human DPP3 mRNA sequence followed by cytometric detection using celigo cell count assay, flow cytometry, wound-healing assay and trans-well assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis-related genes. A xenograft model was applied to the detection of tumor growth and invasion of DPP3-depleted cancer cells in nude mice.Results: DPP3 expression was elevated in esophageal cancer tissues compared with adjacent non-tumor tissues (normal controls) with statistical significance (P<0.05), and associated with poor prognosis of esophageal carcinoma. The DPP3-depletion resulted in a reduced cell proliferation and migration and enhanced cell-cycle arrest and apoptosis of esophageal cancer cells, and lead to the inhibition of tumor growth and invasion in xenograft model. In addition, DPP3-depletion was associated with the upregulation of pro-apoptotic proteins and the downregulation of anti-apoptotic proteins.Conclusions: These findings suggest that DPP3 may promote cell proliferation, migration and survival of esophageal cancer cells in vitro, and tumor growth and invasion of esophageal carcinoma in vivo and this might serve as a molecular target for tumor therapy.

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

2017 ◽  
pp. 4-9
Author(s):  
С.В. Калиш ◽  
С.В. Лямина ◽  
А.А. Раецкая ◽  
И.Ю. Малышев
Keyword(s):  
Tumor Growth ◽  
Culture Medium ◽  
Ehrlich Carcinoma ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
M1 Macrophage ◽  
Ec Cells ◽  
Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

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