scholarly journals Characteristics of TGFBR1–EGFR–CTNNB1–CDH1 Signaling Axis in Wnt-Regulated Invasion and Migration in Lung Cancer

2020 ◽  
Vol 29 ◽  
pp. 096368972096916
Author(s):  
Rong Liu ◽  
Yusui Zhang ◽  
Yuan Ding ◽  
Shuai Zhang ◽  
Long Pan
Keyword(s):  
Lung Cancer ◽  
Wnt Signaling Pathway ◽  
Growth Factor Receptor ◽  
Migration And Invasion ◽  
Migration Ability ◽  
P Values ◽  
Invasion And Migration ◽  
Signaling Axis ◽  
And Migration ◽  
Interfering Rna

This study aimed to explore the characteristics of TGFBR1–epidermal growth factor receptor (EGFR)–CTNNB1–CDH1 axis in regulating the invasion and migration in lung cancer. Using the small interfering RNA technology, EGFR was silenced in H2170 and H1299 cells. Then, the colony formation, migration, and invasion abilities were detected using colony-forming assay and transwell assay. Moreover, the mRNA expression of smad2, smad3, CTNNB1, and CDH1, and the protein expression of TGFBR1, CDH1, and TCF were determined using the real-time polymerase chain reaction and western blotting. The results showed that silencing EGFR could significantly decrease the colony-forming ability in H2170 and H1299. Knocking down EGFR could significantly inhibit the invasion and migration ability of H2179 and H1299. Inhibiting the expression of EGFR could significantly decrease the expression of smad2, smad3, CDH1, and CTNNB1, with all P-values <0.05. In addition, silencing EGFR could markedly decrease the expression of TGFBR1 and CDH1 in H1299 and H2170, with all P-values <0.05. In conclusion, silencing EGFR could significantly regulate the progression of lung cancer via TGFBR1–EGFR–CTNNB1–CDH1 axis in Wnt signaling pathway.

scholarly journals Icotinib-resistant HCC827 cells produce exosomes with mRNA MET oncogenes and mediate the migration and invasion of NSCLC

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Yiming Yu ◽  
Maidinaimu Abudula ◽  
Chaofen Li ◽  
Zhongbo Chen ◽  
Yun Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Cancer Metastasis ◽  
Quantitative Polymerase Chain Reaction ◽  
Migration And Invasion ◽  
Migration Ability ◽  
Acquired Drug Resistance ◽  
Invasion And Migration ◽  
And Migration ◽  
Nsclc Patients

Abstract Background Icotinib has been widely used in patients with non-small cell lung cancer (NSCLC), and have significantly enhanced the overall survival rate of NSCLC patients. However, acquired drug resistance limits its clinical efficacy. Tumor cell-derived exosomes have been reported to participate in various biological processes, including tumor invasion, metastasis and drug resistance. Materials and methods In the present study, drug resistance was measured by MTT assay. Exosomes were extracted from the cell supernatant using ultracentrifugation and identified by exosomal marker. HCC827 cells were treated with exosomes derived from icotinib-resistant (IR) HCC827 to observe the invasion and migration of parent cells. The expression of exo-mRNA was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-PCR). In addition, 10 exo-mRNAs detecting from the plasma and bronchoalveolar lavage fluid (BALF) of NSCLC patients with icotinib treatment were used to establish a new drug resistant-warning formula. Results The oncogene MET into exosomes was identified from icotinib-resistant lung cancer cells, and this was also presented in exosomes in NSCLC patients diagnosed with cancer metastasis after icotinib treatment. The knockdown of MET in exosomes significantly decreased the ability of invasion and migration in HCC827 cells. Conclusion It was suggested that MET might be specifically package and transferred by exosomes to modify the invasion and migration ability of the surrounding icotinib-sensitive cells.

scholarly journals LncRNA HOTAIR Influences the Growth, Migration, and Invasion of Papillary Thyroid Carcinoma via Affection on the miR-488-5p/NUP205 Axis

2020 ◽  
Vol 19 ◽  
pp. 153303382096212
Author(s):  
Feng Xia ◽  
Wei Xia ◽  
Xudong Yu
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
Well Assay ◽  
And Migration

Objective: The study was aim to investigate the effect of HOX transcript antisense RNA (HOTAIR) on the growth, migration, and invasion of papillary thyroid carcinoma (PTC) and its underlying mechanisms. Methods: Cell growth, invasion, and migration was respectively investigated using the MTT assay, trans-well assay, and wound healing assay. The expression of genes and proteins was respectively determined by Western blot analysis and RT-PCR experiments. Results: It was demonstrated that high expression of HOTAIR in PTC cells (BCPAP) and tissues resulted in fast tumor growth and poor survival time of the PTC-bearing mice models. Moreover, overexpression of HOTAIR leaded to markedly enhanced proliferation, migration, and invasion of BCPAP cells. Increase the levels of HOTAIR in BCPAP cells signally down-regulated the miR-488-5p levels which was able of inhibiting the growth rate, increasing the apoptosis rate, and decreasing the invasion/migration ability of BCPAP cells. Further studies indicated that HOTAIR promoted BCPAP cell growth, invasion, and migration mainly through regulating the miR-488-5p/NUP205 axis and the levels of Bcl-2 as well. Conclusion: HOTAIR promoted the growth, migration, and invasion of papillary thyroid carcinoma mainly through regulating the miR-488-5p/NUP205 axis.

scholarly journals LncRNA PLAC 2 downregulated miR-21 in non-small cell lung cancer and predicted survival

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Huan Xia ◽  
Ming Xiu ◽  
Jinying Gao ◽  
Hongyu Jing
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Over Expression ◽  
Nsclc Patients

Abstract Background LncRNA PLAC2 has been characterized as a tumor suppressive lncRNA in glioma. We investigated the role of PLAC2 in non-small cell lung cancer (NSCLC). Methods A total of 187 NSCLC patients were admitted by The First Hospital of Jilin University from December 2010 to December 2014. All the patients were diagnosed by histopathological approaches. Transient cell transfections, RT-qPCR, invasion, and migration ability measurement, were applied for the experiments. Results PLAC2 was down-regulated, while miR-21 was up-regulated in NSCLC tissues compared to non-cancer tissues. Low PLAC2 levels in NSCLC tissues were associated with poor survival of NSCLC patients. PLAC2 and miR-21 were inversely correlated, and PLAC 2 over-expression in NSCLC cells resulted in the down-regulation of miR-21. However, miR-21 over-expression did not significantly affect PLAC2 expression. In addition, PLAC2 over-expression resulted in decreased migration and invasion rates of NSCLC cells. MiR-21 over-expression played the opposite role and attenuated the effects of PLAC2 over-expression. Conclusions In conclusion, lncRNA PLAC2 down-regulated miR-21 in NSCLC and inhibited cancer cell migration and invasion.

scholarly journals Silencing of Estrogen receptor β promotes the invasion and migration of osteosarcoma cells through activating Wnt signaling pathway

2019 ◽  
Author(s):  
Yiping Zhang ◽  
Changchang Yin ◽  
Xufeng Zhou ◽  
Yahua Wu ◽  
Lili Wang
Keyword(s):  
Estrogen Receptor ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Estrogen Receptor Β ◽  
Migration And Invasion ◽  
Metastatic Tumors ◽  
Subcutaneous Tumor ◽  
Invasion And Migration ◽  
And Migration

Abstract Background This study aimed to evaluate the specific roles of Estrogen receptor β (ERβ) on the invasion and migration of osteosarcoma (OS) cells, and explore the regulatory mechanisms relating with Wnt signaling pathway. Methods The expression of ERβ was detected on human OS tissues by quantitative real-time PCR and immunohistochemistry. U2-OS cells were transfected with siRNA-ERβ (si-ERβ) to downrgulate ERβ, and treated with FH535 to inhibit Wnt signaling. The migration and invasion ability was detected by scratch and transwell assay, respectively. The expression of β-catenin, MMP-7 and MMP-9 was detected by Western blot. Subcutaneous tumor-bearing model was established by injection of U2-OS cells into mice, and the tumor volumes were measured. Orthotopic transplantation model was established by transplantation of tumor tissues into the liver of mice, and the metastatic tumors were counted. Results ERβ was downregulated in human OS tissues and U2-OS cells. The transfection of si-ERβ significantly increased the scratch healing rate, the number of invasion cells, and the expression of β-catenin, MMP-7 and MMP-9 in U2-OS cells. The injection of si-ERβ-transfected U2-OS cells into mice significantly increased the subcutaneous tumor volume, the expression of β-catenin, MMP-7 and MMP-9, and the number of metastatic tumors in liver tissues. The promoting effects of si-ERβ on the invasion and migration of U2-OS cells were significantly reversed by FH535 in vitro and vivo. Conclusions Silencing of ERβ promotes the invasion and migration of OS cells via activating Wnt signaling pathway.

scholarly journals miR-182-5p improves the viability, mitosis, migration, and invasion ability of human gastric cancer cells by down-regulating RAB27A

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Yuling Li ◽  
Shudong Chen ◽  
Zhengfei Shan ◽  
Liyan Bi ◽  
Shengqiang Yu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Gene Assay ◽  
And Migration

We investigated the effect of miR-182-5p on the viability, proliferation, invasion, and migration ability of human gastric cells by regulating the expression of RAB27A. Real-time PCR assay was used to detect the expression of miR-182-5 and RAB27A in human gastric carcinoma tissues, para-carcinoma tissues, and different cell lines. Western blotting was also used to determine the RAB27A expression in both tissues and cell lines. We chose the HGC-27 cell line as experiment subject as it demonstrated the highest miR-182-5p level. HGC-27 cells were transfected with different vectors and the cell viability, mitosis, invasion, and migration ability were measured through MTT assay, flow cytometry (FCM) analysis, Transwell assay, and wound healing assay. In comparison with the normal tissues, miR-182-5p is expressed at a higher level in gastric cancer (GC) tissues, while RAB27A is expressed at a lower level in cancerous tissues. The down-regulation of miR-182-5p and up-regulation of RAB27A can significantly decrease the viability, migration, invasion, and mitosis of HGC-27 cells. The target relationship between miR-182-5p and RAb27A was confirmed through a dual-luciferase reporter gene assay and Western blot assay. miR-182-5p enhances the viability, mitosis, migration, and invasion of human GC cells by down-regulating RAB27A.

scholarly journals LncRNA WT1-AS downregulates lncRNA UCA1 to suppress non-small cell lung cancer and predicts poor survival

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yanhui Wan ◽  
Da Yao ◽  
Fuyuan Fang ◽  
Youyu Wang ◽  
Guodong Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Poor Survival ◽  
Invasion And Migration ◽  
And Migration ◽  
Nsclc Patients

Abstract Background LncRNA WT1-AS inhibits gastric cancer, while its role in other cancers is unknown. We investigated the role of WT1-AS in non-small cell lung cancer (NSCLC). Methods Sixty-six NSCLC patients (40 males and 26 females; 36 to 68 years old; mean age 52.7 ± 6.4 years old) were selected from the 178 NSCLC patients operated on for lung cancer between 2010 and 2013. RT-qPCR was used to analyze the expression of lncRNA. Overexpression experiments were performed to assess interactions between lncRNAs. CCK-8 assay was carried to evaluate the roles of WT1-AS and UCA1 in regulating cell proliferation. Cell invasion and migration assays were performed to assess the roles of WT1-AS and UCA1 in regulating cell invasion and migration. Western-blot was performed to illustrate the effect of WT1-AS and UCA1 in EMT. Results WT1-AS was downregulated in NSCLC and was correlated with poor survival. The expression of WT1-AS in NSCLC was not correlated with clinical stages. LncRNA UCA1 was upregulated in cancer tissues and inversely correlated with WT1-AS. Overexpression of UCA1 did not affect WT1-AS, while overexpression of WT1-AS led to inhibited expression of UCA1. Overexpression of UCA1 resulted in increased proliferation, EMT, migration and invasion of NSCLC cells, while overexpression of WT1-AS showed opposite effects. In addition, overexpression of UCA1 inhibited the role of overexpression of WT1-AS. Conclusions Therefore, overexpression of WT1-AS may inhibit the cell proliferation and EMT to decrease cell migration and invasion of NSCLC cells by downregulating UCA1.

Mogroside V Inhibits Hyperglycemia-induced Lung Cancer Cells Metastasis through Reversing EMT and Damaging Cytoskeleton

2019 ◽  
Vol 19 (11) ◽  
pp. 885-895
Author(s):  
Jun Chen ◽  
Demin Jiao ◽  
Yu Li ◽  
Chunyan Jiang ◽  
Xiali Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Cellular Proliferation ◽  
Rho Gtpase ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Background: Diabetes Mellitus (DM) accelerates progress of lung cancer. Hyperglycemia, a critical feature of DM, promotes lung cancer metastasis. Mogroside V is a triterpenoid glycoside from Siraitia grosvenorii. Interestingly, mogroside V not only plays an anti-diabetic role, but also has anti-tumor effects. Objective: In this study, we investigated the metastatic efficiency of mogroside V in lung cancer cells cultured in hyperglycemia. Methods: Two lung cancer cell lines-A549 and H1299 were cultured in normoglycemia (5.5mM glucose) and hyperglycemia (25mM glucose). Cellular proliferation was tested by MTT, invasion was examined by transwell assay, migration was measured by wound healing assay, cytoskeleton was stained by Phalloidin-TRITC and the expressions of EMT markers and Rho-GTPase family protein were detected by western blot. Results: Hyperglycemia promoted the invasion and migration of A549 and H1299 cells compared with normoglycemia. Mogroside V inhibited the hyperglycemia-induced invasion and migration. Hyperglycemia promoted epithelial-mesenchymal transition (EMT), while mogroside V could reverse this process through up-regulating E-Cadherin expression and down-regulating N-Cadherin, Vimentin, Snail expressions. Furthermore, mogroside V fractured microfilaments and reduced Rho A, Rac1, Cdc42 and p-PAK1 expressions under hyperglycemic conditions. Conclusion: These results suggest that mogroside V inhibits hyperglycemia-induced lung cancer cells migration and invasion through reversing EMT and damaging cytoskeleton.

scholarly journals Mitofusin 2 Expression in Placental Tissues of Preeclamptic Patients and Its Correlations with Trophoblast Invasion and Placental Hypoxia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoyan Wang
Keyword(s):  
Trophoblast Invasion ◽  
Migration And Invasion ◽  
Transwell Assay ◽  
Mitofusin 2 ◽  
Invasion And Migration ◽  
Qrt Pcr ◽  
Protein Expressions ◽  
Normal Women ◽  
And Migration ◽  
Interfering Rna

The researcher aimed to detect mitofusin 2 (Mfn2) expression in the placental tissues of preeclampsia (PE) patients and correlations with trophoblast invasion and placental hypoxia. Mfn2 mRNA expressions in placental tissues from PE and healthy pregnant women were detected by qRT-PCR. Trophoblast cells JEG-3 were transfected with small-interfering RNA-Mfn2 (si-Mfn2). Proliferation was tested by CCK-8 and colony formation assays. Invasion and migration were determined with Transwell assay. Mfn2, HIF-1á, HPH-1 and leptin protein expressions were detected by Western blotting. Mfn2 protein had strong positive and weak negative expressions in normal and PE women, respectively. Mfn2 mRNA expression in PE women was lower than that in normal women (P<0.05). Compared with control and si- NC groups, si-Mfn2 group had lower proliferation, migration and invasion abilities, as well as HIF-1á, HPH-1 and leptin expressions (P<0.05). Mfn2 expression in the placental tissues of PE women obviously decreases, which inhibits trophoblast invasion and triggers placental hypoxia.

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