scholarly journals MicroRNA-148b Inhibits the Malignant Biological Behavior of Melanoma by Reducing Sirtuin 7 Expression Levels

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Rui Sun ◽  
Meiliang Guo ◽  
Xiaojing Fan ◽  
Qinqin Meng ◽  
Dingfen Yuan ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Therapeutic Approach ◽  
Ectopic Expression ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Malignant Cells ◽  
Carcinogenic Effect ◽  
Proliferation And Metastasis ◽  
Tumor Growth And Metastasis

There is growing evidence that microRNA-148b (miR-148b) can inhibit the growth of malignant cells while sirtuin 7 (SIRT7) may perform its carcinogenic effect by deacetylating H3K18. This study investigated the mechanism of miR-148b/SIRT7 on how it affects the malignant biological behavior of melanoma. It was established that the expression of miR-148b was downregulated in melanoma while that of SIRT7 was upregulated but negatively regulated by miR-148b through binding to the 3 ′ UTR of SIRT7. Ectopic expression of miR-148b reduced the proliferation, migration, and invasion of melanoma cells, but SIRT7 reversed these functions of miR-148b. Moreover, tumor growth and metastasis experiments showed that miR-148b could significantly suppress proliferation and metastasis of melanoma in vivo. Overall, miR-148b inhibits the malignant biological behavior of melanoma by reducing the expression level of SIRT7. The development of miR-148b as a novel potential therapeutic approach for melanoma may be possible in the future.

scholarly journals Kinesin Family Member 18A (KIF18A) Contributes to the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Fu-Tao Chen ◽  
Fu-Kuan Zhong
Keyword(s):  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Clinical Stage ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Tumor Growth And Metastasis

Objective. To determine the expression levels of KIF18A in lung adenocarcinoma and its relationship with the clinicopathologic features of patients undergoing radical colectomy and explore the potential role in the progression of lung adenocarcinoma. Methods. Immunohistochemical assays were performed to explore the expression levels of KIF18A in 82 samples of lung adenocarcinoma and corresponding normal tissues. According to the levels of KIF18A expression in lung adenocarcinoma tissue samples, patients were classified into the KIF18A high expression group and low expression group. Clinical data related to the perioperative clinical features (age, gender, smoking, tumor size, differentiation, clinical stage, and lymph node metastasis), the potential correlation between KIF18A expression levels, and clinical features were analyzed, and the effects of KIF18A on lung adenocarcinoma cell proliferation, migration, and invasion were measured by colony formation assay, MTT assay, wound healing assay, and transwell assays. The possible effects of KIF18A on tumor growth and metastasis were measured in mice through tumor growth and tumor metastasis assays in vivo. Results. KIF18A in lung adenocarcinoma tissues. Further, KIF18A was significantly associated to clinical characteristic features including the tumor size (P=0.033) and clinical stage (P=0.041) of patients with lung adenocarcinoma. Our data also investigated that KIF18A depletion dramatically impairs the proliferation, migration, and invasion capacity of lung adenocarcinoma cells in vitro and inhibits tumor growth and metastasis in mice. Conclusions. Our study reveals the involvement of KIF18A in the progression and metastasis of lung adenocarcinoma and provides a novel therapeutic target for the treatment of lung adenocarcinoma.

scholarly journals LncRNA DANCR promotes the proliferation, migration, and invasion of tongue squamous cell carcinoma cells through miR-135a-5p/KLF8 axis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ying Zheng ◽  
Bowen Zheng ◽  
Xue Meng ◽  
Yuwen Yan ◽  
Jia He ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Ectopic Expression ◽  
Underlying Mechanism ◽  
Tongue Squamous Cell Carcinoma ◽  
Migration And Invasion

Abstract Background Tongue squamous cell carcinoma (TSCC) is a most invasive cancer with high mortality and poor prognosis. It is reported that lncRNA DANCR has implications in multiple types of cancers. However, its biological role and underlying mechanism in TSCC progress are not well elucidated. Methods Our present study first investigated the function of DANCR on the proliferation, migration and invasion of TSCC cells by silencing or overexpressing DANCR. Further, the miR-135a-5p-Kruppel-like Factor 8 (KLF8) axis was focused on to explore the regulatory mechanism of DANCR on TSCC cell malignant phenotypes. Xenografted tumor growth using nude mice was performed to examine the role of DANCR in vivo. Results DANCR knockdown reduced the viability and inhibited the migration and invasion of TSCC cells in vitro, while ectopic expression of DANCR induced opposite effects. In vivo, the tumor growth and the expression of matrix metalloproteinase (MMP)-2/9 and KLF8 were also blocked by DANCR inhibition. In addition, we found that miR-135-5p directly targeted DANCR, which was negatively correlated with DANCR on TSCC progression. Its inhibition reversed the beneficial effects of DANCR silence on TSCC malignancies. Furthermore, the expression of KLF8 evidently altered by both DANCR and miR-135a-5p. Silencing KLF8 using its specific siRNA showed that KLF8 was responsible for the induction of miR-135a-5p inhibitor on TSCC cell malignancies and MMP-2/9 expression. Conclusions These findings, for the first time, suggest that DANCR plays an oncogenic role in TSCC progression via targeting miR-135a-5p/KLF8 axis, which provides a promising biomarker and treatment approach for preventing TSCC.

scholarly journals Dimethyl fumarate restores apoptosis sensitivity and inhibits tumor growth and metastasis in CTCL by targeting NF-κB

Blood ◽  
2016 ◽  
Vol 128 (6) ◽  
pp. 805-815 ◽  
Author(s):  
Jan P. Nicolay ◽  
Karin Müller-Decker ◽  
Anne Schroeder ◽  
Markus Brechmann ◽  
Markus Möbs ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Growth ◽  
Therapeutic Approach ◽  
Dimethyl Fumarate ◽  
Specific Cell ◽  
Key Points ◽  
Tumor Growth And Metastasis ◽  
Novel Therapeutic

Key Points DMF induces specific cell death in CTCL cells and inhibits CTCL tumor growth and metastasis in vivo via inhibition of NF-κB. DMF therefore represents a promising, nontoxic novel therapeutic approach to treating CTCL.

scholarly journals GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lin Tan ◽  
Weiming Qu ◽  
Dajun Wu ◽  
Minji Liu ◽  
Qian Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Underlying Mechanism ◽  
Promoting Effect ◽  
Promote Tumor Growth ◽  
Proliferation And Metastasis ◽  
Tumor Growth And Metastasis ◽  
Cell Proliferation And Metastasis

GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of tumor-promoting effect of GRHL3 in colorectal cancer (CRC), which is involved in the MEK1/2 pathway. The expression of GRHL3 was measured in CRC and adjacent normal tissue using qPCR and immunohistochemical staining. Lentivirus-mediated knockdown expression of GRHL3 was performed in the CRC cell line HT29. Cell proliferation and metastasis were assayed in vitro, and tumorigenicity was investigated in vivo. We found higher GRHL3 expression in colorectal cancer, which was negatively correlated with patients’ prognosis. Results from studies in vitro and in vivo indicated that downregulation of GRHL3 expression inhibited tumor growth and metastasis and inhibited the activation of the MEK1/2 pathway. The effect of GRHL3 downexpression was the same as that of MEK1/2 antagonists on suppression of tumor growth and metastasis. Our results suggested that GRHL3 may act as an oncogene to promote tumor growth and metastasis via the MEK pathway in colorectal cancer.

scholarly journals Andrographolide Suppresses the Growth and Metastasis of Luminal-Like Breast Cancer by Inhibiting the NF-κB/miR-21-5p/PDCD4 Signaling Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Junchen Li ◽  
Lixun Huang ◽  
Zinan He ◽  
Minggui Chen ◽  
Yi Ding ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Tumor Model ◽  
Antitumor Agent ◽  
Migration And Invasion ◽  
Antitumor Effects ◽  
Tumor Growth And Metastasis

Tumor growth and metastasis are responsible for breast cancer-related mortality. Andrographolide (Andro) is a traditional anti-inflammatory drug used in the clinic that inhibits NF-κB activation. Recently, Andro has been found in the treatment of various cancers. Andro inhibits breast cell proliferation and invasion and induces apoptosis via activating various signaling pathways. Therefore, the underlying mechanisms with regard to the antitumor effects of Andro still need to be further confirmed. Herein, a MMTV-PyMT spontaneous luminal-like breast cancer lung metastatic transgenic tumor model was employed to estimate the antitumor effects of Andro on breast cancer in vivo. Andro significantly inhibited tumor growth and metastasis in MMTV-PyMT mice and suppressed the cell proliferation, migration, and invasion of MCF-7 breast cancer cells in vitro. Meanwhile, Andro significantly inhibited the expression of NF-κB, and the downregulated NF-κB reduced miR-21-5p expression. In addition, miR-21-5p dramatically inhibited the target gene expression of programmed cell death protein 4 (PDCD4). In the current study, we demonstrated the potential anticancer effects of Andro on luminal-like breast cancer and indicated that Andro inhibits the expression of miR-21-5p and further promotes PDCD4 via NF-κB suppression. Therefore, Andro could be an antitumor agent for the treatment of luminal-like breast cancer in the clinic.

scholarly journals Long Non-coding RNA SNHG12, a New Therapeutic Target, Regulates miR-199a-5p/Klotho to Promote the Growth and Metastasis of Intrahepatic Cholangiocarcinoma Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Hong-Guo Yang ◽  
Tian-peng Wang ◽  
Sheng-an Hu ◽  
Chao-zhou Hu ◽  
Cheng-hang Jiang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Intrahepatic Cholangiocarcinoma ◽  
Therapeutic Target ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Direct Binding ◽  
Proliferation And Metastasis ◽  
Long Non Coding Rna

Background: Small nucleolar RNA host gene 12 (SNHG12) is a newly identified long non-coding RNA (lncRNA) whose involvements have been explored in several cancers. Our study aimed to explore the functions of SNHG12 on intrahepatic cholangiocarcinoma (ICC) progression and its interaction with miR-199a-5p and Klotho.Methods: RT-PCR was performed to examine the expressions of SNHG12, miR-199a-5p and Klotho in ICC cells. Cell counting kit-8 (CCK-8), colony formation assays and transwell assays were applied to analyze the proliferation, migration and invasion of ICC cells. Luciferase assays, RIP assays and RNA pull-down assays were carried out to demonstrate the direct binding relationships among SNHG12, miR-199a-5p and Klotho. The xenograft nude models were applied to test the effects of SNHG12 on ICC tumor growth.Results: The expression of SNHG12 and Klotho was distinctly increased in ICC cells, while miR-199a-5p expressions were decreased. Functionally, the silence of SNHG12 inhibited the proliferation and metastasis of ICC cells, while miR-199a-5p overexpression exhibited an opposite result. Mechanistically, Knockdown of SNHG12 significantly suppressed the expressions of miR-199a-5p by sponging it, and then increased Klotho expression. The final in vivo experiments suggested that the silence of SNHG12 distinctly inhibited tumor growth.Conclusion: Our findings indicated that SNHG12 inhibited cell proliferation and metastasis process of ICC cells through modulating the miR-199a-5p/Klotho axis and it is expected to become a potential therapeutic target for ICC.

scholarly journals NFAT1 enhances the effects of tumor-associated macrophages on promoting malignant melanoma growth and metastasis

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Hao Liu ◽  
Liping Yang ◽  
Min Qi ◽  
Jianglin Zhang
Keyword(s):  
Malignant Melanoma ◽  
Tumor Growth ◽  
Critical Role ◽  
Macrophage Infiltration ◽  
Migration And Invasion ◽  
Tumor Associated Macrophages ◽  
Human Malignant Melanoma ◽  
Tumor Growth And Metastasis ◽  
Melanoma Growth

Tumor-associated macrophages (TAMs) play substantial roles in tumor growth, invasion, and metastasis. Nuclear factor of activated T cell (NFAT1) has been shown to promote melanoma growth and metastasis in vivo. We herein aim to investigate whether NFAT1 is capable to promote melanoma growth and metastasis by influencing TAM properties. Melanoma-conditioned TAMs were obtained from human monocytes after incubation with conditioned medium from A375 cell culture. The phenotype of the macrophages was detected. Cell proliferation, migration, and invasion were evaluated. Human malignant melanoma tissues exhibited increased CD68+-macrophage infiltration and NFAT1 expression compared with the normal pigmented nevus tissues. Melanoma-conditioned TAMs displayed M2-like phenotype. Melanoma-conditioned TAMs also promoted proliferation, migration, and invasion of human malignant melanoma cell lines A375 and WM451. Furthermore, NFAT1 expression in TAMs was significantly increased compared with the M0 group. NFAT1 overexpression significantly strengthened the melanoma-conditioned TAM-mediated promotion of cell migration and invasion in A375 and WM451 cells, whereas NFAT1 knockdown exerted the opposite effects. Moreover, NFAT1 overexpression in melanoma-conditioned TAMs promoted CD68+-macrophage infiltration, tumor growth, and metastasis in vivo. NFAT1 may play a critical role in enhancing the TAM-mediated promotion of growth and metastasis in malignant melanoma.

scholarly journals FGF-induced LHX9 regulates the progression and metastasis of osteosarcoma via FRS2/TGF-β/β-catenin pathway

Cell Division ◽  
2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Shuang-Qing Li ◽  
Chao Tu ◽  
Lu Wan ◽  
Rui-Qi Chen ◽  
Zhi-Xi Duan ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Growth ◽  
Migration And Invasion ◽  
Transcriptional Level ◽  
Invasion And Metastasis ◽  
Real Time Quantitative Pcr ◽  
Tumor Growth Factor ◽  
Tumor Growth And Metastasis ◽  
Related Proteins

Abstract Background Fibroblast growth factor (FGF) and tumor growth factor-β (TGFβ) have emerged as pivotal regulators during the progression of osteosarcoma (OS). LHX9 is one crucial transcription factor controlled by FGF, however, its function in OS has not been investigated yet. Methods The expression of LHX9, FRS2, BMP4, TGF-beta R1, SMAD2, beta-catenin and metastasis-related proteins was measured by real-time quantitative PCR (RT-qPCR) and Western blot. CCK-8 assay and colony formation assay were employed to determine the proliferation of OS cells, while scratch wound healing assay and transwell assay were used to evaluate their migration and invasion, respectively. In vivo tumor growth and metastasis were determined by subcutaneous or intravenous injection of OS cells into nude mice. Results LHX9 expression was evidently up-regulated in OS tumor tissues and cell lines. Knockdown of LHX9 impaired the proliferation, migration, invasion and metastasis of OS cells. Mechanistically, LHX9 silencing led to the down-regulation of BMP-4, β-catenin and metastasis-related proteins, which was also observed in beta-catenin knockdown OS cells. By contrast, FRS2 knockdown conduced to the up-regulation of LHX9, BMP4, β-catenin and TGF-βR1, while TGF-beta inhibition repressed the expression of LHX9 and metastasis-related proteins. Additionally, let-7c modulates LHX9 and metastasis-related proteins by suppressing TGF-beta R1 expression on transcriptional level. Conclusions This study revealed LHX9 was essential for the proliferation, migration, invasion, and metastasis of OS cells via FGF and TGF-β/β-catenin signaling pathways.

scholarly journals circTLK1 facilitates the proliferation and metastasis of renal cell carcinoma by regulating miR-495-3p/CBL axis

2021 ◽  
Vol 16 (1) ◽  
pp. 362-374
Author(s):  
Xiangli Lei ◽  
Meiling Yang ◽  
Zhifang Xiao ◽  
Heng Zhang ◽  
Shuai Tan
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Growth ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Proliferation And Metastasis

Abstract Renal cell carcinoma (RCC) is a common urological malignancy. Circular RNAs (circRNAs) have been confirmed to play an important regulatory role in various cancers. This study aimed to investigate the role and potential mechanism of circTLK1 (hsa_circ_0004442) in RCC. The levels of circTLK1, Cbl proto-oncogene (CBL), and microRNA-495-3p (miR-495-3p) were detected by quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation, cycle arrest and apoptosis, migration, and invasion were assessed by colony formation, flow cytometry, scratch, and transwell assays. The levels of E-cadherin and Vimentin were measured by western blot. The targeting relationship between miR-495-3p and miR-495-3p or CBL was verified by dual-luciferase reporter assay. Tumor growth in vivo was evaluated by xenograft assay. The results found that circTLK1 and CBL were up-regulated in RCC tissues and cells. Silencing of circTLK1 or CBL inhibited proliferation and metastasis and accelerated apoptosis in RCC cells. In addition, circTLK1 directly bound to miR-495-3p, and CBL was the target of miR-495-3p. circTLK1 sponged miR-495-3p to increase CBL expression. Moreover, knockdown of circTLK1 suppressed tumor growth in vivo. In conclusion, down-regulation of circTLK1 restrained proliferation and metastasis and promoted apoptosis in RCC cells by modulating miR-495-3p/CBL axis.

CCNE1 promotes progression and is associated with poor prognosis in lung adenocarcinoma

2021 ◽  
Vol 22 ◽  
Author(s):  
Guoliang Ma ◽  
Lulu Yang ◽  
Jing Dong ◽  
Lili Zhang
Keyword(s):  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Annexin V ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Cyclin E1 ◽  
Tumor Growth And Metastasis

Background : Mounting evidence has shown that Cyclin E1 (CCNE1) facilitates various carcinoma progression, but its function in lung adenocarcinoma (LUAD) remains unclear. Objective: Our study aims to explore the significance of CCNE1 in clinical progression and study its biological functions in LUAD. Methods: CCNE1 expressions in LUAD specimens and cells were detected through quantitative realtime polymerase chain reaction (qRT-RCR) and western blot. An immunohistochemistry technique was used to detect CCNE1 expression to explore its association with clinical parameters. The LUAD cells with stable knockdown of CCNE1 were constructed by small interfering RNA. The effect of CCNE1 on LUAD cells proliferation and apoptosis was evaluated through Cell Counting Kit-8 (CCK-8), colony formation, and Annexin V/propidium iodide (AV-PI) assays, respectively. The cell migration and invasion were evaluated by Wound-healing and Transwell assays, respectively. The xenograft and lung metastasis mouse models were introduced to analyze how CCNE1 knockdown affects tumor growth and tumor metastasis. Results: CCNE1 expression was upregulated in LUAD tissue and cells. CCNE1 knockdown inhibited LUAD cellular malignant behavior in vitro and reduced tumor growth and metastasis in vivo. High expression of CCNE1 was correlated with big tumor size, cancer stage, lymph node metastasis, and poor prognosis. Conclusions: CCNE1 overexpression promotes LUAD growth, metastasis, and forebode poor prognosis: it can serve as a new prognostic marker of LUAD.

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