In vitro generation of tumour-specific lymphocyte reactivity to colonic carcinoma cells

1987 ◽  
Vol 25 (3) ◽  
Author(s):  
Maria Kuppner ◽  
Stephen Wilkinson ◽  
Elizabeth Casson ◽  
Oleg Eremin
Keyword(s):  
Carcinoma Cells ◽  
Colonic Carcinoma ◽  
Lymphocyte Reactivity

Fate of antibody-neocarzinostatin conjugates bound to human colonic carcinoma cells in vitro

1992 ◽  
Vol 28 (9-10) ◽  
pp. 569-570 ◽  
Author(s):  
Takashi Yokota ◽  
Kazuya Kitamura ◽  
Toshiharu Yamaguchi ◽  
Toshio Takahashi
Keyword(s):  
Carcinoma Cells ◽  
Colonic Carcinoma

scholarly journals Preparation and Characterization of a Novel Triple Composite Scaffold Containing Silk Fiborin, Chitosan, and Alginate for 3D Culture of Colonic Carcinoma Cells In Vitro

2020 ◽  
Vol 26 ◽  
Author(s):  
Xianhao Su ◽  
Liang Chen ◽  
Shanliang Han ◽  
Gengming Niu ◽  
Jun Ren ◽  
...  
Keyword(s):  
Composite Scaffold ◽  
3D Culture ◽  
Carcinoma Cells ◽  
Colonic Carcinoma

In vitro and in silico anticancer evaluation of a medicinal mushroom, Ganoderma neo‐japonicum Imazeki, against human colonic carcinoma cells

2020 ◽  
Author(s):  
Meng‐Fei Lau ◽  
Kek‐Heng Chua ◽  
Vikineswary Sabaratnam ◽  
Umah Rani Kuppusamy
Keyword(s):  
In Silico ◽  
Carcinoma Cells ◽  
Colonic Carcinoma ◽  
Medicinal Mushroom

The influence of extracts from Rubus caesius leaves on human colon carcinoma cells cultured in vitro

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
R Paduch ◽  
M Tomczyk ◽  
A Wiater ◽  
A Dudek ◽  
M Pleszczynska ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Cells Cultured

The role of α2, αv and β1 Integrins in cell growth of hepatocellular carcinoma cells in vitro

2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
M Juratli ◽  
A Schnitzbauer ◽  
R Blaheta ◽  
W Bechstein
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Β1 Integrins

Overexpression of p62 Induces Autophagy and Promotes Proliferation, Migration and Invasion of Nasopharyngeal Carcinoma Cells through Promoting ERK Signaling Pathway

2020 ◽  
Vol 20 (8) ◽  
pp. 624-637 ◽  
Author(s):  
Qiong Wu ◽  
Manlin Xiang ◽  
Kun Wang ◽  
Zhen Chen ◽  
Lu Long ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Clinical Analysis ◽  
Carcinoma Cells ◽  
Immunofluorescent Staining ◽  
Clinicopathological Parameters ◽  
Migration And Invasion ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Potential Biomarker

Background: Increasing evidence has shown that p62 plays an important role in tumorigenesis. However, relatively little is known about the association between p62 and tumor invasion and metastasis; in addition, its role in NPC (nasopharyngeal carcinoma, NPC) has been rarely investigated. Objective: To investigate the effect of p62 on tumorigenesis and metastasis in nasopharyngeal carcinoma. Methods: Western blotting, immunofluorescent staining and immunohistochemistry were used to evaluate p62 protein expression. Subsequently, cell viability, colony formation, migration, invasion and autophagy assays were performed. anti-p62 autoantibodies in sera were detected by ELISA. These data were correlated with clinicopathological parameters. Results: We confirmed that p62 was significantly up-regulated in NPC tissues. Furthermore, high expression of p62 was observed in NPC cell lines, and especially in the highly metastatic 5-8F cells. In vitro, down-regulation of p62 inhibited proliferation, clone forming ability, autophagy, migration, and invasion in 5-8F cells, whereas p62 overexpression resulted in the opposite effects in 6-10B cells. Moreover, we confirmed that p62 promotes NPC cell proliferation, migration, and invasion by activating ERK (extracellular signal-regulated kinase, ERK). Clinical analysis indicated that high p62 expression correlates with lymph node and distant metastasis (P<0.05). Serum anti-p62 autoantibodies were increased in NPC patients and levels were associated with metastasis. Conclusion : Our data establish p62 targeting ERK as potential determinant in the NPC, which supplies a new pathway to treat NPC. Furthermore, p62 is a potential biomarker which might be closely related to the tumorigenesis and metastasis in NPC.

In Vitro and In Vivo Effect of Palladacycles: Targeting A2780 Ovarian Carcinoma Cells and Modulation of Angiogenesis

2021 ◽  
Vol 60 (6) ◽  
pp. 3939-3951
Author(s):  
Francisco Reigosa-Chamorro ◽  
Luís R. Raposo ◽  
Paula Munín-Cruz ◽  
M. Teresa Pereira ◽  
Catarina Roma-Rodrigues ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Carcinoma Cells

scholarly journals Characterization of LDD-2633 as a Novel RET Kinase Inhibitor with Anti-Tumor Effects in Thyroid Cancer

2021 ◽  
Vol 14 (1) ◽  
pp. 38
Author(s):  
Hyo Jeong Lee ◽  
Pyeonghwa Jeong ◽  
Yeongyu Moon ◽  
Jungil Choi ◽  
Jeong Doo Heo ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Carcinoma ◽  
Kinase Inhibitor ◽  
Point Mutations ◽  
Carcinoma Cells ◽  
Medullary Thyroid ◽  
Potent Inhibition ◽  
Kinase Inhibitory Activity

Rearranged during transfection (RET), a receptor tyrosine kinase, is activated by glial cell line-derived neurotrophic factor family ligands. Chromosomal rearrangement or point mutations in RET are observed in patients with papillary thyroid and medullary thyroid carcinomas. Oncogenic alteration of RET results in constitutive activation of RET activity. Therefore, inhibiting RET activity has become a target in thyroid cancer therapy. Here, the anti-tumor activity of a novel RET inhibitor was characterized in medullary thyroid carcinoma cells. The indirubin derivative LDD-2633 was tested for RET kinase inhibitory activity. In vitro, LDD-2633 showed potent inhibition of RET kinase activity, with an IC50 of 4.42 nM. The growth of TT thyroid carcinoma cells harboring an RET mutation was suppressed by LDD-2633 treatment via the proliferation suppression and the induction of apoptosis. The effects of LDD-2633 on the RET signaling pathway were examined; LDD-2633 inhibited the phosphorylation of the RET protein and the downstream molecules Shc and ERK1/2. Oral administration of 20 or 40 mg/kg of LDD-2633 induced dose-dependent suppression of TT cell xenograft tumor growth. The in vivo and in vitro experimental results supported the potential use of LDD-2633 as an anticancer drug for thyroid cancers.

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