Ethanol Extracts of Fruiting Bodies of<i>Antrodia cinnamomea</i>Suppress CL1-5 Human Lung Adenocarcinoma Cells Migration by Inhibiting Matrix Metalloproteinase-2/9 through ERK, JNK, p38, and PI3K/Akt Signaling Pathways

Chen, Ying Yi; Liu, Fon Chang; Chou, Pei Yu; Chien, Yi Chung; Chang, Wun Shaing Wayne; Huang, Guang Jhong; Wu, Chieh Hsi; Sheu, Ming Jyh

doi:10.1155/2012/378415

Cited by 44 publications

(47 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Prior results have shown that elevated MMP-2 and -9 was observed in late stages of cancer, which could be a prognostic factor in several human cancers (17). Furthermore, prevention of lung cancer metastasis by inhibition of MMP-2 and/or MMP-9 by bioactive compounds isolated from plants and herbs has been previously demonstrated (18,19). Extracts from Antrodia cinnamomea displayed antimetastatic effects by the supersession of MMP-2 and -9 activities (18,19).…”

Section: Discussionmentioning

confidence: 93%

“…Furthermore, prevention of lung cancer metastasis by inhibition of MMP-2 and/or MMP-9 by bioactive compounds isolated from plants and herbs has been previously demonstrated (18,19). Extracts from Antrodia cinnamomea displayed antimetastatic effects by the supersession of MMP-2 and -9 activities (18,19). Furthermore, fisetin and myricetin inhibited the nuclear translocation of NF-κB, c-Fos and c-Jun, decreased the expression and activities of MMP-2 and urokinase-type plasminogen activator, and eventually attenuated the migration and metastasis of lung A549 cells (20,21).…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Chang

Lai

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Lung cancer is among the most common causes of cancer-related mortality. It has a high mortality rate and resistance to chemotherapy due to its high metastatic potential. Naringenin, a bioactive compound identified in several fruits, displays anti-inflammatory and antitumor effects. Furthermore, naringenin mitigates the migration of several human cancer cell types. However, the effects of naringenin on lung cancer remain unclear. The current study investigated the mechanisms of naringenin on the migration of lung cancer A549 cells. The results indicate that significant alteration in A549 cell proliferation was observed in response to naringenin (0-300 µM) treatment for 24 and 48 h. Furthermore, a dose-dependent migration inhibition of A549 in the presence of naringenin was observed by healing and transwell migration assays. In addition, a zymography assay revealed that naringenin exhibited a concentration-dependent inhibition of matrix metalloproteinase (MMP)-2 and -9 activities. Furthermore, naringenin also inhibited the activities of AKT in a dose-dependent manner. These observations indicated that naringenin inhibited the migration of lung cancer A549 cells through several mechanisms, including the inhibition of AKT activities and reduction of MMP-2 and -9 activities.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Chang

Lai

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…Recently, many natural extracts have been demonstrated to inhibit migration in various cancer cells via PI3K/AKT, a downstream pathway of FAK [34][35][36][37]. The activity of RhoGTPase proteins is also regulated by the function of activated Akt (pAkt) [38][39][40].…”

Section: Resultsmentioning

confidence: 99%

A bibenzyl from Dendrobium ellipsophyllum inhibits migration in lung cancer cells

Chaotham

Chanvorachote

2015

J Nat Med

View full text Add to dashboard Cite

Metastatic cancer cells have been shown to have aggressive behaviors accounting for the high incidence of chemotherapeutic failure and mortality. Because migration and invasion are crucial behaviors for cancer cell dissemination, promising compounds exhibiting potential antimigration effects are of interest for metastasis-based therapeutic approaches. This study aimed to evaluate the activity of a bibenzyl, 4,5,4'-trihydroxy-3,3'-dimethoxybibenzyl (TDB), isolated from Dendrobium ellipsophyllum Tang and Wang, in the suppression of migration in human lung cancer cells. TDB at nontoxic concentrations (1 and 5 µM) significantly inhibited the motility of lung cancer cells in scratch-wound assay. Chemotaxis-induced migration and invasion assays also revealed that the cell motility dramatically diminished in the cells treated with 1-5 µM TDB. Western blot analysis provided the underlying molecular mechanism, showing that TDB reduced such cell migration and invasion by decreasing migration-regulating proteins, including integrins αv, α4, β1, β3 and β5, as well as downstream signaling proteins, such as activated focal adhesion kinase (pFAK), activated Ras-related C3 botulinum toxin substrate 1 (Rac1-GTP) and cell division control protein 42 (Cdc42). As the presence of cellular protrusion, called filopodia, has been indicated as a hallmark of migrating cells, we showed that the reduction of the mentioned proteins correlated well with the disappearance of filopodia. In summary, this study demonstrates the promising activity of TDB and its mechanism in the inhibition of lung cancer cell migration, which might be useful for encouraging the development of this compound for antimetastatic approaches.

show abstract

“…An increasing number of studies have shown that the PI3K/AKT signaling pathway may modulate the expression of MMPs, as well as TIMPs, to promote the degradation of ECM proteins, and this mechanism was essential for invasion of human tumors, including lung cancer (13,23). To the best of our knowledge, allicin has been confirmed to inhibit the PI3K/AKT signaling pathway in the HepG2 cell line; however, it remains unknown whether such an effect also exists in lung adenocarcinoma (17).…”

Section: Discussionmentioning

confidence: 99%

Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling

et al. 2017

View full text Add to dashboard Cite

Abstract. Allicin, the main active principle associated with Allium sativum chemistry, has various antitumor activities. However, to the best of our knowledge, there is no available information to address the anti-invasive effect and associated mechanism in lung adenocarcinoma. In the present study, cell viability assay, cell adhesion assay, western blot analysis, Transwell migration and invasion assays and reverse transcription-quantitative polymerase chain reaction were performed. Allicin was identified to inhibit the adhesion, invasion and migration of lung adenocarcinoma cells in a dose-dependent manner, accompanied by decreasing mRNA and protein levels of matrix metalloproteinase (MMP)-2 and MMP-9. Conversely, the mRNA and protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 were increased in a dose-dependent manner. Furthermore, it was revealed that allicin treatment significantly suppressed the phosphorylation of AKT (P<0.05), but not the total protein expression of AKT. Combined treatment with LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K)/AKT signaling, and allicin led to the synergistic reduction of MMP-2 and MMP-9 expression, followed by an increase in TIMP-1 and TIMP-2 expression. The invasive capabilities of lung adenocarcinoma cells were also suppressed. However, insulin-like growth factor-1 (an activator of PI3K/AKT signaling) reversed the effects of allicin on cell invasion and expression of MMP-2, MMP-9, TIMP-1 and TIMP-2. The present study concluded that allicin may inhibit invasion of lung adenocarcinoma cells by altering TIMP/MMP balance, via reducing the activity of the PI3K/AKT signaling pathway. This indicated that allicin may be recognized as an anti-invasive agent for lung adenocarcinoma treatment. IntroductionLung cancer is the predominant reason of cancer-associated mortality in developed and developing countries. Lung adenocarcinoma is the most common histological type of lung cancer, and accounts for ~50% of all lung cancers (1). Although the management and treatment of surgery, radiotherapy and chemotherapy have improved, the therapeutic efficacy is poor. One of the major reasons is the lack of adequate treatment against lung adenocarcinoma invasion (2,3). Therefore, the development of novel adjuvant therapeutic strategies specifically targeting the progression of invasion is of critical importance for improving the prognosis of patients with lung adenocarcinoma.Invasion occurs through a complex pathophysiological process involving multiple genetic alterations (4,5). Matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, play an important role in the invasion process of numerous malignant tumors by degrading the basement membrane and extracellular matrix (ECM) (6-8). Previous studies have suggested that MMP-2 and MMP-9 are associated with invasion in lung cancer (4,5). In addition, numerous studies have demonstrated that MMPs may be regulated by tissue inhibitor of metalloproteinase (TIMP) (6,9). Disturbing the balance of MMPs and TIMPs ma...

show abstract

Ethanol Extracts of Fruiting Bodies ofAntrodia cinnamomeaSuppress CL1-5 Human Lung Adenocarcinoma Cells Migration by Inhibiting Matrix Metalloproteinase-2/9 through ERK, JNK, p38, and PI3K/Akt Signaling Pathways

Cited by 44 publications

References 48 publications

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

A bibenzyl from Dendrobium ellipsophyllum inhibits migration in lung cancer cells

Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling

Contact Info

Product

Resources

About