scholarly journals An in vitro correlation of metastatic capacity and dual mechanostimulation

PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0207490
Author(s):  
Indrajyoti Indra ◽  
Alexander N. Gasparski ◽  
Karen A. Beningo
Keyword(s):  
Metastatic Capacity

Juniperus communis Suppresses Melanoma Tumorigenesis by Inhibiting Tumor Growth and Inducing Apoptosis

2019 ◽  
Vol 47 (05) ◽  
pp. 1171-1191 ◽  
Author(s):  
Hong-Wei Gao ◽  
Xiao-Fan Huang ◽  
Tzi-Peng Yang ◽  
Kai-Fu Chang ◽  
Ling-Wen Yeh ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Death Rate ◽  
Tumor Burden ◽  
Autocrine Signaling ◽  
Juniperus Communis ◽  
Common Skin ◽  
Metastatic Capacity ◽  
Induction Of Apoptosis

Melanoma, which has a high metastatic capacity and death rate, is a common skin cancer in Western countries. The purpose of this study was to address whether Juniperus communis (JCo) extract is effective in the suppression of melanoma and to elucidate the anticancer mechanisms involved in vitro and in vivo. The antitumor capacities of JCo extract on tumor suppression and toxicity were evaluated and the results demonstrated that the tumor burden was reduced via mediation of cell cycle, reduction of autocrine signaling, and induction of apoptosis. Moreover, JCo extract significantly prolonged the survival rate of the test subjects with only low pathological and physiological toxicity. Additionally, JCo extract also reduced cancer stem cell-related angiogenic and metastatic proteins in the process of tumor elimination. Based on these results, this study suggests that JCo extract suppresses tumor growth and induces apoptosis, and JCo extract may be useful for the prevention of melanoma tumorigenesis.

scholarly journals MPC1 Deficiency Promotes CRC Liver Metastasis via Facilitating Nuclear Translocation of β-Catenin

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Guang-Ang Tian ◽  
Chun-Jie Xu ◽  
Kai-Xia Zhou ◽  
Zhi-Gang Zhang ◽  
Jian-Ren Gu ◽  
...  
Keyword(s):  
Tumor Metastasis ◽  
Nuclear Translocation ◽  
Tca Cycle ◽  
Mitochondrial Pyruvate Carrier ◽  
Human Sample ◽  
Metastatic Capacity ◽  
Tcga Dataset

Accumulating evidence has pointed out that metastasis is the leading cause of death in several malignant tumor, including CRC. During CRC, metastatic capacity is closely correlated with reprogrammed energy metabolism. Mitochondrial Pyruvate Carrier 1 (MPC1), as the carrier of transporting pyruvate into mitochondria, linked the glycolysis and TCA cycle, which would affect the energy production. However, the specific role of MPC1 on tumor metastasis in CRC remains unexplored. Here, by data mining of genes involved in pyruvate metabolism using the TCGA dataset, we found that MPC1 was significantly downregulated in CRC compared to nontumor tissues. Similar MPC1 expression pattern was also found in multiple GEO datasets. IHC staining in both human sample and AOM/DSS induced mouse CRC model revealed significant downregulation of MPC1. What is more, we found that MPC1 expression was gradually decreased in normal tissue, primary CRC, and metastasis CRC. Additionally, poor prognosis emerged in the MPC1 low expression patients, especially in patients with metastasis. Following, functional tests showed that MPC1 overexpression inhibited the motility of CRC cells in vitro and MPC1 silencing enhanced liver metastases in vivo. Furthermore, we uncovered that decreased MPC1 activated the Wnt/β-catenin pathway by promoting nuclear translocation of β-catenin to mediate the expression of MMP7, E-cadherin, Snail1, and myc. Collectively, our data suggest that MPC1 has the potential to be served as a promising biomarker for diagnosis and a therapeutic target in CRC.

scholarly journals Autotaxin upregulated by STAT3 activation contributes to invasion in pancreatic neuroendocrine neoplasms

2018 ◽  
Vol 7 (12) ◽  
pp. 1299-1307 ◽  
Author(s):  
Linfei Yang ◽  
Xiao Yu ◽  
Yongchao Yang
Keyword(s):  
Western Blot ◽  
Cell Line ◽  
Neuroendocrine Neoplasms ◽  
Pancreatic Neuroendocrine Neoplasms ◽  
Node Metastasis ◽  
Stat3 Phosphorylation ◽  
Elevated Expression ◽  
Tumour Node Metastasis Stage ◽  
Metastatic Capacity

Although the upregulation of autotaxin (ATX) is associated with many solid tumours, its role in pancreatic neuroendocrine neoplasms (pNEN) has not been well elucidated. The expression of ATX in pNEN tissues and pNEN cell line BON1 was analysed by Western blot, PCR and immunocytochemistry upon exposure to interleukin-6 (IL-6). Additionally, pNEN cell line BON1 was transfected with siRNAs against ATX or signal transducer and activator of transcription 3 (STAT3) and assessed by in vitro invasion assays. The following results were obtained. The expression of ATX in pNEN tissues was significantly increased compared with that in normal pancreatic tissues. High ATX expression was strongly correlated with tumour grade, lymph node metastasis and tumour-node-metastasis stage. Furthermore, ATX downregulation notably inhibited the metastatic capacity of pNEN cells, whereas STAT3 knockdown was found to downregulate the expression of ATX. ATX expression was upregulated in BON1 cells upon stimulation with IL-6, and this was accompanied by activation/phosphorylation of STAT3. Western blot analysis of human pNEN tissue extracts confirmed increased ATX expression and STAT3 phosphorylation with elevated expression levels of IL-6. In conclusion, ATX is upregulated in pNEN and is correlated with the metastatic capacity of pNEN cells, potentially via interaction with STAT3 activation.

scholarly journals Ancient Adversary – HERV-K (HML-2) in Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Eoin Dervan ◽  
Dibyangana D. Bhattacharyya ◽  
Jake D. McAuliffe ◽  
Faizan H. Khan ◽  
Sharon A. Glynn
Keyword(s):  
Tumour Progression ◽  
Endogenous Retroviruses ◽  
Open Reading Frames ◽  
Human Endogenous Retroviruses ◽  
Viral Particles ◽  
Metastatic Capacity ◽  
Coding Capacity ◽  
Reading Frames

Human endogenous retroviruses (HERV), ancient integrations of exogenous viruses, make up 8% of our genome. Long thought of as mere vestigial genetic elements, evidence is now accumulating to suggest a potential functional role in numerous pathologies including neurodegenerative diseases, autoimmune disorders, and multiple cancers. The youngest member of this group of transposable elements is HERV-K (HML-2). Like the majority of HERV sequences, significant post-insertional mutations have disarmed HERV-K (HML-2), preventing it from producing infectious viral particles. However, some insertions have retained limited coding capacity, and complete open reading frames for all its constituent proteins can be found throughout the genome. For this reason HERV-K (HML-2) has garnered more attention than its peers. The tight epigenetic control thought to suppress expression in healthy tissue is lost during carcinogenesis. Upregulation of HERV-K (HML-2) derived mRNA and protein has been reported in a variety of solid and liquid tumour types, and while causality has yet to be established, progressively more data are emerging to suggest this phenomenon may contribute to tumour growth and metastatic capacity. Herein we discuss its potential utility as a diagnostic tool and therapeutic target in light of the current in vitro, in vivo and clinical evidence linking HERV-K (HML-2) to tumour progression.

scholarly journals Acquisition of high metastatic capacity after in vitro fusion of a nonmetastatic tumor line with a bone marrow-derived macrophage.

1984 ◽  
Vol 160 (5) ◽  
pp. 1579-1584 ◽  
Author(s):  
L Larizza ◽  
V Schirrmacher ◽  
E Pflüger
Keyword(s):  
Bone Marrow ◽  
Parental Line ◽  
Primary Tumors ◽  
Lymphoma Line ◽  
Visceral Metastases ◽  
Metastatic Capacity ◽  
T Lymphoma ◽  
Hybrid Lines

A low metastatic, thioguanine-resistant murine T lymphoma line (EbTGR) was hybridized in vitro, with the help of polyethylene glycol, with syngeneic bone marrow-derived macrophages. Two HAT-resistant hybrid lines (Eb-F1 and Eb-F2) were obtained from independent fusion cultures. A cytogenetic analysis revealed that most of the macrophage chromosomes except No. 12 had segregated or become rearranged 60 d after fusion, a time at which the cell lines had become stabilized in culture. Syngeneic mice inoculated subcutaneously with the tumor macrophage hybrid lines developed, very quickly, visceral metastases and died after less than 2 wk, while those inoculated with the parental line lived for greater than 6 wk and developed only localized, large primary tumors. The metastatic hybridomas expressed a similar tumor antigen as a spontaneous, in vivo derived, high metastatic variant (ESb) of the same tumor. This suggests that ESb cells might have arisen from a spontaneous fusion with a host macrophage.

p53 increases experimental metastatic capacity of murine carcinoma cells

1988 ◽  
Vol 8 (5) ◽  
pp. 2078-2081
Author(s):  
J Pohl ◽  
N Goldfinger ◽  
A Radler-Pohl ◽  
V Rotter ◽  
V Schirrmacher
Keyword(s):  
P53 Protein ◽  
P53 Gene ◽  
Metastatic Potential ◽  
Carcinoma Cells ◽  
Growth Potential ◽  
Growth Properties ◽  
Metastatic Capacity ◽  
Similar Growth ◽  
Intravenous Inoculation

Transfection of a cloned p53 gene into a murine bladder carcinoma cell with a low metastatic capacity led to elevated levels of p53 protein in clonal transfectants. After intravenous inoculation into syngeneic mice, p53-transfected clones showed significantly increased metastatic potential in comparison with control transfectants. The observed change did not seem to be due to a change in growth potential per se since the cell lines showed similar growth properties in vitro.

scholarly journals p53 increases experimental metastatic capacity of murine carcinoma cells.

1988 ◽  
Vol 8 (5) ◽  
pp. 2078-2081 ◽  
Author(s):  
J Pohl ◽  
N Goldfinger ◽  
A Radler-Pohl ◽  
V Rotter ◽  
V Schirrmacher
Keyword(s):  
P53 Protein ◽  
P53 Gene ◽  
Metastatic Potential ◽  
Carcinoma Cells ◽  
Growth Potential ◽  
Growth Properties ◽  
Metastatic Capacity ◽  
Similar Growth ◽  
Intravenous Inoculation

Transfection of a cloned p53 gene into a murine bladder carcinoma cell with a low metastatic capacity led to elevated levels of p53 protein in clonal transfectants. After intravenous inoculation into syngeneic mice, p53-transfected clones showed significantly increased metastatic potential in comparison with control transfectants. The observed change did not seem to be due to a change in growth potential per se since the cell lines showed similar growth properties in vitro.

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