scholarly journals Cathepsin L increases invasion and migration of B16 melanoma

2007 ◽  
Vol 7 (1) ◽  
pp. 8 ◽  
Author(s):  
Zhen Yang ◽  
James L Cox
Keyword(s):  
Cathepsin L ◽  
B16 Melanoma ◽  
Invasion And Migration ◽  
And Migration

scholarly journals TFE3 Regulates the Function of the Autophagy-Lysosome Pathway to Drive the Invasion and Metastasis of Papillary Thyroid Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Hongsheng Lu ◽  
Chumeng Zhu ◽  
Yanyun Ruan ◽  
Lilong Fan ◽  
Kena Wei ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Cathepsin L ◽  
Clinicopathological Characteristics ◽  
Vital Role ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
And Migration

Background. Accumulating evidence shows that autophagy plays a vital role in tumor occurrence, development, and metastasis and even determines tumor prognosis. However, little is known about its role in papillary thyroid carcinoma (PTC) or the potentially oncogenic role of TFE3 in regulating the autophagy-lysosome system. Methods. Immunohistochemistry and quantitative real-time PCR (qRT-PCR) were used to examine the expression of TFE3, P62/SQSTM1, and LC3 in PTC and paracancerous tissues. TFE3, P62/SQSTM1, LC3, cathepsin L (CTSL), and cathepsin B (CTSB) were evaluated using Western blot analysis. After inducing TFE3 overexpression by plasmid or TFE3 downregulation by small interfering RNA (siRNA) transfection, MTT, wound healing, and cell migration and invasion assays were used to verify the effects on invasion, migration, and the levels of autophagy-lysosome system-related proteins such as P62/SQSTM1, LC3, CTSL, and CTSB. Results. TFE3 was overexpressed in PTC tissues compared with paracancerous tissues. Analysis of the clinicopathological characteristics of PTC patients showed that high TFE3 expression was significantly correlated with lymph node metastasis. TFE3 overexpression in the PTC cell lines KTC-1 and BCPAP promoted proliferation, invasion, and migration, while TFE3 knockdown had the opposite effects. Furthermore, we identified a positive relationship among the expression levels of TFE3, P62/SQSTM1, LC3, CTSL, and CTSB. We found that silencing TFE3 inhibited the expression of P62/SQSTM1, LC3, CTSL, and CTSB in PTC cells. However, TFE3 overexpression had the opposite effects. Conclusions. The present study provided evidence for the underlying mechanisms by which TFE3 induces autophagy-lysosome system activity in PTC.

K-ras mutation promotes ionizing radiation-induced invasion and migration of lung cancer in part via the Cathepsin L/CUX1 pathway

2018 ◽  
Vol 362 (2) ◽  
pp. 424-435 ◽  
Author(s):  
Long Wang ◽  
Yifan Zhao ◽  
Yajie Xiong ◽  
Wenjuan Wang ◽  
Yao Fei ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ionizing Radiation ◽  
Cathepsin L ◽  
Ras Mutation ◽  
Invasion And Migration ◽  
Radiation Induced ◽  
And Migration

Cathepsin L is involved in X-ray-induced invasion and migration of human glioma U251 cells

2017 ◽  
Vol 29 ◽  
pp. 181-191 ◽  
Author(s):  
Yajie Xiong ◽  
Wenjun Ji ◽  
Yao Fei ◽  
Yifan Zhao ◽  
Long Wang ◽  
...  
Keyword(s):  
Cathepsin L ◽  
Human Glioma ◽  
X Ray ◽  
Invasion And Migration ◽  
And Migration ◽  
U251 Cells

Influence of fibroblasts on the invasion and migration of highly or weakly metastatic b16 melanoma cells

1994 ◽  
Vol 56 (6) ◽  
pp. 867-873 ◽  
Author(s):  
Ikuo Saiki ◽  
Jun Murataxd ◽  
Junya Yoneda ◽  
Hideo Kobayashi ◽  
Ichiro Azuma
Keyword(s):  
Melanoma Cells ◽  
B16 Melanoma ◽  
Invasion And Migration ◽  
B16 Melanoma Cells ◽  
And Migration

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

Dynamic Changes of Collagen Ⅳ During Cancer Invasion and Migration: Pulse Mode

2013 ◽  
Vol 40 (10) ◽  
pp. 1056
Author(s):  
Min FANG ◽  
Jing-Ping YUAN ◽  
Chun-Wei PENG ◽  
Shao-Ping LIU ◽  
Yan LI
Keyword(s):  
Cancer Invasion ◽  
Pulse Mode ◽  
Dynamic Changes ◽  
Invasion And Migration ◽  
And Migration

Wnt/beta-catenin and PI3K/Akt/mTOR Signaling Pathways in Glioblastoma: Two Main Targets for Drug Design: A Review

2020 ◽  
Vol 26 (15) ◽  
pp. 1729-1741 ◽  
Author(s):  
Seyed H. Shahcheraghi ◽  
Venant Tchokonte-Nana ◽  
Marzieh Lotfi ◽  
Malihe Lotfi ◽  
Ahmad Ghorbani ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Chemotherapy Resistance ◽  
Wnt Signaling Pathway ◽  
Therapeutic Interventions ◽  
Beta Catenin ◽  
Clinical Prognosis ◽  
Invasion And Migration ◽  
And Migration

: Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging technologies, surgery, and adjuvant treatments, the clinical prognosis of patients with GBM remains persistently unfavorable. The signaling pathways and the regulation of growth factors of glioblastoma cells are very abnormal. The various signaling pathways have been suggested to be involved in cellular proliferation, invasion, and glioma metastasis. The Wnt signaling pathway with its pleiotropic functions in neurogenesis and stem cell proliferation is implicated in various human cancers, including glioma. In addition, the PI3K/Akt/mTOR pathway is closely related to growth, metabolism, survival, angiogenesis, autophagy, and chemotherapy resistance of GBM. Understanding the mechanisms of GBM’s invasion, represented by invasion and migration, is an important tool in designing effective therapeutic interventions. This review will investigate two main signaling pathways in GBM: PI3K/Akt/mTOR and Wnt/beta-catenin signaling pathways.

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