PAR-3 Knockdown Enhances Adhesion Rate of PANC-1 Cells via Increased Expression of Integrinαv and E-Cadherin

Segal, Liora; Katz, Liora S.; Shapira, Hagit; Sandbank, Judith; Geras‐Raaka, Elizabeth; Gershengorn, Marvin C.; Oron, Yoram

doi:10.1371/journal.pone.0093879

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…Cadherins are considered to be the most important group of molecules involved in cell-cell and cell-matrix adhesion (28). Decreased expression of E-cadherin has been associated with more advanced tumor stages and grades for lung (29), gastric tract (30), breast (31), bladder (32), colorectal (33) and prostate (34) cancer.…”

Section: Discussionmentioning

confidence: 99%

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Jiang

Hardie

et al. 2017

Oncology Letters

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Abstract. Metastasis of lung carcinoma cells is a major cause of organ failure and mortality of patients with lung cancer. Lung mast cells are a type of immune cell which reside in the respiratory mucosa. High numbers of mast cells are associated with the majority of common types of cancer; however, the effects of mast cells on cancer remain unclear. In the present study, the effects of mast cell chymase (MCC) on the proliferation and adhesion of the lung carcinoma cell lines A549 and H520 was investigated. After 24 h of treatment, the highest dose of MCC (50 mU/ml) decreased the proliferation rate of A549 and H520 cells, whereas the lowest dose of MCC (5 mU/ml) resulted in a small increase in the viability. A549 cells treated with MCC lost adhesion ability in a MCC dose-dependent manner; however, these detached cells were able to regrow when transferred to a fresh culture. The protein expression of epithelial (E-) cadherin, p53 and p21 in A549 lung carcinoma cells were detected by western blot analysis. The results of the present study revealed that, following 24 h of treatment, the expression level of E-cadherin was decreased, the p53 tumor suppressor protein was expressed in limited quantities and the expression of p21 was decreased. Zymography was used to examine the effects of MCC on the expression and activation of matrix metalloproteinase-9 (MMP-9) in A549 and H520 cells. The expression of MMP-9 in the two cell lines was time-and MCC dose-dependent. The results of the present study demonstrated that MCC stimulated lung carcinoma cell proliferation and adhesion, as well as regulated E-cadherin expression and the cell cycle, all of which are associated with cancer metastasis. Therefore, MCC may be a potential candidate for lung carcinoma therapy.

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Section: Discussionmentioning

confidence: 99%

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Jiang

Hardie

et al. 2017

Oncology Letters

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“…An adhesion rate assay was performed according to the previous report [29]. Briefly, 30 lL Matrigel (2 mg/mL) was added into the 96 well plate at room temperature.…”

Section: Adhesion Rate Of C6 Cells To Extracellular Matrixmentioning

confidence: 99%

Vinorelbine cationic liposomes modified with wheat germ agglutinin for inhibiting tumor metastasis in treatment of brain glioma

Xiao

Cheng

Xie

et al. 2018

Artificial Cells, Nanomedicine, and Biotechnology

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Glioma is the most common primary malignant brain tumor with a poor prognosis. The application of chemotherapeutic drugs is limited due to the existence of blood-brain barrier and serious side effects. Liposomes have been proven to be a stable and useful drug delivery system for tumors. In this paper, WGA (wheat germ agglutinin) modified vinorelbine cationic liposomes had been successfully constructed for treating glioma. In the liposomes, WGA was modified on the liposomal surface for crossing the blood-brain barrier and increasing the targeting effects, 3-(N-(N 0 , N 0-dimethylaminoethane) carbamoyl) cholesterol (DC-Chol) was used as cationic material and vinorelbine was encapsulated in the aqueous core of liposomes to inhibit tumor metastasis and kill tumor cells. Studies were performed on C6 cells in vitro and were verified in brain glioma-bearing mice in vivo. Results in vitro demonstrated that the targeting liposomes could induce C6 cells apoptosis, promote drugs across the blood-brain barrier, inhibit the metastasis of tumor cells and increase targeting effects to tumor cells. Meanwhile, action mechanism studies showed that the targeting liposomes could down-regulate PI3K, MMP-2, MMP-9 and FAK to inhibit tumor metastasis. Results in vivo exhibited that the targeting liposomes displayed an obvious antitumor efficacy by accumulating selectively in tumor site and exhibited low toxicity to blood system and major organs. Hence, WGA modified vinorelbine cationic liposomes might provide a safe and efficient therapy strategy for glioma.

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“…PAR3 was expressed in kidney and liver cancer ( 14 , 15 ). In human pancreatic adenocarcinoma PANC-1 cells, knockdown of PAR3 markedly enhanced cell migration and invasion ( 16 ). PAR4 was also expressed in multiple tumors.…”

Section: Introductionmentioning

confidence: 99%

PAR4 overexpression promotes colorectal cancer cell proliferation and migration

et al. 2018

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Protease-activated receptor 4 (PAR4), a member of the G-protein-coupled receptor family, was previously identified to be involved in the progression of cancer. Previous study revealed that the expression of PAR4 was increased in colorectal cancer tissues compared with the associated normal tissues, particularly in positive lymph node and poorly differentiated types of cancer. We hypothesized that PAR4 serves a function in the progression of colorectal cancer. In the present study, overexpression of PAR4 in colorectal cancer LoVo cells promoted proliferation, anchorage-independent growth and migration. In vivo, PAR4 increased LoVo cell tumorgenicity. In contrast, knockdown of PAR4 in HT-29 cells decreased proliferation, anchorage-independent growth and migration. Mechanistic studies revealed that PAR4 increased the phosphorylation of extracellular-signal-regulated kinase 1/2 in colorectal cancer cells, which is the potential molecular mechanism that promotes cellular proliferation and migration. Taken together, the results of the present study indicated that overexpression of PAR4 promoted colorectal cancer cell proliferation, survival and metastasis, indicating that PAR4 is a promising therapeutic target for preventing colon cancer progression.

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PAR-3 Knockdown Enhances Adhesion Rate of PANC-1 Cells via Increased Expression of Integrinαv and E-Cadherin

Cited by 7 publications

References 20 publications

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Vinorelbine cationic liposomes modified with wheat germ agglutinin for inhibiting tumor metastasis in treatment of brain glioma

PAR4 overexpression promotes colorectal cancer cell proliferation and migration

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