scholarly journals MiRNA-128-3p Restrains Malignant Melanoma Cell Malignancy by Targeting NTRK3

2021 ◽  
Vol 10 ◽  
Author(s):  
Xinxin Zhou ◽  
Jiayuan He ◽  
Qingyuan Wang ◽  
Teng Ma
Keyword(s):  
Malignant Melanoma ◽  
Tumor Suppressor ◽  
Molecular Mechanisms ◽  
Malignant Progression ◽  
Neurotrophin Receptor ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Current Survey ◽  
Low Levels ◽  
Complementary Binding

The functions of non-coding RNA, including microRNA (miRNA), have attracted considerable attention in the field of oncology, In this report, we examined the roles and molecular mechanisms of miR-128-3p, as related to the biological behaviors of malignant melanoma (MM). We found that miR-128-3p was expressed in low levels in these MM cells and may serve as a tumor suppressor by inhibiting proliferation, migration, and invasion, as well as inducing apoptosis in these MM cells. Moreover, neurotrophin receptor 3 (NTRK3), which serves as an oncogene that can enhance malignant behaviors of MM cells, was up-regulated in MM cells. Our current survey disclosed a complementary binding between miR-128-3p and the NTRK3 3′ untranslated regions (3′-UTR), while luciferase activities of NTRK3 3′-UTR were restrained by miR-128-3p in 293T cells. The effects of pre-miR-128-3p and sh-NTRK3 as well as anti-miR-128-3p and NTRK3(+) appeared to function synergistically in producing malignant progression. Moreover, there were possible to have counteracted effects for pre-miR-128-3p and NTRK3(+) in malignant progression. These findings established that miR-128-3p can function as a tumor suppressor by inhibiting carcinogenesis of the oncogene, NTRK3. Collectively, miR-128-3p and NTRK3 genes participate in modulating the malignant behavior of MM, and may represent new therapeutic targets for MM.

scholarly journals Long non-coding RNA HULC affects the proliferation, apoptosis, migration, and invasion of mesenchymal stem cells

2018 ◽  
Vol 243 (13) ◽  
pp. 1074-1082 ◽  
Author(s):  
Xiujun Li ◽  
Jiali Wang ◽  
Yuchen Pan ◽  
Yujun Xu ◽  
Dan Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Liver Cancer ◽  
Clinical Application ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Therapeutic Effects ◽  
Non Coding Rna ◽  
And Function ◽  
Long Non Coding Rna

Further studies on the molecular mechanisms of mesenchymal stem cells in the maintenance of growth and function are essential for their clinical application. Growing evidence has shown that long non-coding RNAs (lncRNAs) play an important role in the regulation of mesenchymal stem cells. Recently, it is reported that highly upregulated in liver cancer (HULC), with another lncRNA MALAT-1, accelerated liver cancer stem cell growth. The regulating role of MALAT-1 in mesenchymal stem cells has been investigated. However, the effects of HULC on the mesenchymal stem cells are unknown. In this study, we overexpressed HULC in mesenchymal stem cells derived from umbilical cord and analyzed the cell phenotypes, proliferation, apoptosis, migration, invasion and differentiation of mesenchymal stem cells. We found that overexpression of HULC significantly promotes cell proliferation through promoting cell division and inhibits cell apoptosis. HULC-overexpressed mesenchymal stem cells migrate and invade faster than control mesenchymal stem cells. HULC has no effect on phenotypes and differentiation of mesenchymal stem cells. Furthermore, we found that the expression of HULC in mesenchymal stem cells could be reduced by several inflammatory factors, including TNF-α, TGF-β1, and R848. Taken together, our data demonstrated that HULC has a vital role in the growth and function maintenance of mesenchymal stem cells without affecting differentiation. Impact statement Exploring the molecular mechanisms of growth and function in MSCs is the key to improve their clinical therapeutic effects. Currently, more and more evidence show that the long non-coding RNA (lncRNA) plays an important role in the growth, stemness and function of MSCs.Both HULC and MALAT1 are the earliest discovered LNCRNAs, which are closely related to tumor growth. All of them can promote the growth of liver cancer stem cells. Previously, we have studied the effects of MALAT1 on the growth and function of MSCs. In this study, we focused on the effects of HULC on MSCs. We elucidated the effects of HULC on the growth and differentiation of MSCs, and explored the relationship between inflammatory stimuli and HULC expression in MSCs. Our findings provide a new molecular target for the growth and clinical application of MSCs.

The Role of Tumor-related LncRNA PART1 in cancer

2021 ◽  
Vol 27 ◽  
Author(s):  
Jinlan Chen ◽  
Enqing Meng ◽  
Yexiang Lin ◽  
Yujie Shen ◽  
Chengyu Hu ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
Toll Like Receptor ◽  
Non Coding Rna ◽  
Regulated Expression ◽  
The One ◽  
Long Non Coding Rna

Background: As we all know, long non-coding RNA (lncRNA) affects tumor progression, which has caused a great upsurge in recent years. It can also affect the growth, migration, and invasion of tumors. When we refer to the abnormal expression of lncRNA, we will find it associated with malignant tumors. In addition, lncRNA has been proved to be a key targeted gene for the treatment of some diseases. PART1, a member of lncRNA, has been reported as a regulator in the process of tumor occurrence and development. This study aims to reveal the biological functions, specific mechanisms, and clinical significance of PART1 in various tumor cells. Methods: Through the careful search of PUBMED, the mechanisms of the effect of PART1 on tumorigenesis and development are summarized. Results: On the one hand, the up-regulated expression of PART1 plays a tumor-promoting role in tumors, including lung cancer, prostate cancer, bladder cancer and so on. On the other hand, PART1 is down-regulated in gastric cancer, glioma and other tumors to play a tumor inhibitory role. In addition, PART1 regulates tumor growth mainly by targeting microRNA such as miR-635, directly regulating the expression of proteins such as FUS/EZH2, affecting signal pathways such as the Toll-like receptor pathway, or regulating immune cells. Conclusion: PART1 is closely related to tumors by regulating a variety of molecular mechanisms. In addition, PART1 can be used as a clinical marker for the early diagnosis of tumors and plays an important role in tumor-targeted therapy.

Molecular Regulatory Roles of Long Non-coding RNA HOTTIP: An Overview in Gastrointestinal Cancer

2021 ◽  
Vol 21 ◽  
Author(s):  
Ummi Zulaiqha Hamid ◽  
Maw Shin Sim ◽  
Rhanye Mac Guad ◽  
Vetriselvan Subramaniyan ◽  
Mahendran Sekar ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Diagnostic Value ◽  
Migration And Invasion ◽  
Cellular Functions ◽  
Poor Overall Survival ◽  
Gi Cancer ◽  
Non Coding Rna ◽  
Gi Cancers ◽  
Cancer Phenotypes

: Gastrointestinal (GI) cancers presented an alarmingly high number of new cancer cases worldwide and highly characterised with poor prognosis. The poor overall survival is mainly due to late detection and emerging challenges in treatment, particularly chemoresistance. Thus, the identification of novel molecular targets in GI cancer is highly regarded as the main focus. Recently, long non-coding RNAs (lncRNAs) have been discovered as a potential novel molecular target for combating cancer, as it is highly associated with carcinogenesis and has a great impact on cancer progression. Amongst lncRNAs, HOTIIP has demonstrated a prominent oncogenic regulation in cancer progression, particularly in GI cancers, including oesophageal cancer, gastric cancer, hepatocellular carcinoma, pancreatic cancer and colorectal cancer. This review aimed to present a focused update on the regulatory roles of HOTTIP in GI cancer progression and chemoresistance, as well as deciphering the associated molecular mechanisms underlying their impact on cancer phenotypes and chemoresistance and the key molecules involved. It has been reported that it regulates the expression of various genes and proteins in GI cancers that impacts on the cellular functions, including proliferation, adhesion, migration and invasion, apoptosis, chemosensitivity and tumour differentiation. Furthermore, HOTTIP was also discovered to have a higher diagnostic value as compared to existing diagnostic biomarkers. In overall, HOTTIP has presented itself as a novel therapeutic target and potential diagnostic biomarker in the development of GI cancer treatment.

scholarly journals Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Anqiang Yang ◽  
Handong Wang ◽  
Xiaobing Yang
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Human glioma is one of the malignant tumors of the central nervous system (CNS). Its prognosis is poor, which is due to its genetic heterogeneity and our poor understanding of its underlying molecular mechanisms. The present study aimed to assess the relationship between plasmacytoma variant translocation 1 (PVT1) and enhancer of zeste homolog 2 (EZH2), and their effects on the proliferation and invasion of glioma cells. The expression levels of PVT1 and EZH2 in human glioma tissues and cell lines were measured using quantitative RT-PCR (qRT-PCR). Then, after siRNA-PVT1 and entire PVT1 sequence vector transfection, we determined the regulation roles of PVT1 in the proliferation, apoptosis, migration, and invasion of glioma cells. We found that the expression levels of both PVT1 and EZH2 were up-regulated in human glioma tissues and cell lines, and positively correlated with glioma malignancy. And, silencing of PVT1 expression resulted in decreased proliferation, increased apoptosis, and decreased migration and invasion. In addition, exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion. These data inferred that long non-coding RNA PVT1 could be served as an indicator of glioma prognosis, and PVT1–EZH2 regulatory pathway may be a novel therapeutic target for treating glioma.

scholarly journals Overexpression of Long Non-Coding RNA ZXF2 Promotes Lung Adenocarcinoma Progression Through c-Myc Pathway

2015 ◽  
Vol 35 (6) ◽  
pp. 2360-2370 ◽  
Author(s):  
Ze-Tian Yang ◽  
Zhihong Li ◽  
Xian-Guo Wang ◽  
Tao Tan ◽  
Frank Yi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Tumor Progression ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Potential Interaction ◽  
Migration And Invasion ◽  
Relative Expression Level ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objective: To investigate the expression of long non-coding RNA ZXF2 in lung adenocarcinoma tissues and its effect on cell proliferation, migration and invasion. Methods: Forty pairs of cancerous and adjacent non-cancerous lung adenocarcinoma specimens were collected for the studies. Quantitative real-time PCR was used to analyze the expression of ZXF2 in tumor tissues and adjacent normal tissues. The expression of ZXF2 was correlated with patients' clinico-pathological data. Molecular pathway controlled by ZXF2 was explored by using small interfering RNA (siRNA) technology. CCK-8 cell proliferation assay, flow cytometry analysis and transwell assays were used to evaluate cell proliferation, migration and invasion. Results: The expression of ZXF2 was 2 fold or higher in 27 out of 40 (67.5%) cases of lung adenocarcinoma specimens than that in non-cancerous tissues (P<0.05). The relative expression level of ZXF2 was positively correlated with tumor lymph node metastasis (χ2=8.485, P<0.05) and poor prognosis of the patients (p=0.0217). In order to explore the molecular mechanisms of ZXF2 mediated tumor progression, ZXF2 expression was inhibited by siRNA in A549 cells, a highly aggressive and metastatic lung adenocarcinoma cell line. We found that siRNA-ZXF2 treatment inhibited cell proliferation (P<0.01) leading to cell cycle arrest (P<0.01). The cell migration and invasion were suppressed by siRNA-ZXF2 treatment (P<0.01). Further biochemical studies revealed that the knockdown of ZXF2 led to down regulation of c-Myc signaling. Conclusion: ZXF2 was overexpressed in lung adenocarcinoma tissues and the high expression of ZXF was closely related to tumor progression through c-Myc related pathway. Given the fact that both ZXF2 and c-Myc are located in the same chromosome 8q24.2 loci, the potential interaction between ZXF2 and c-Myc might be a novel target for treatment of lung adenocarcinoma.

scholarly journals The Association of microRNA-34a With High Incidence and Metastasis of Lung Cancer in Gejiu and Xuanwei Yunnan

2021 ◽  
Vol 11 ◽  
Author(s):  
Yan Chen ◽  
Chun Hou ◽  
Liu-xin Zhao ◽  
Qiu-chen Cai ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Yunnan Province ◽  
Molecular Mechanisms ◽  
Small Cell Lung Carcinoma ◽  
Regulatory Gene ◽  
Squamous Carcinoma ◽  
Migration And Invasion ◽  
Cell Lung Carcinoma ◽  
Tumorigenesis And Progression

The incidence and associated mortality of lung cancer in tin miners in Gejiu County and farmers in Xuanwei Country, Yunnan Province have been very high in the world. Current published literatures on the molecular mechanisms of lung cancer initiation and progression in Gejiu and Xuanwei County are still controversial. Studies confirmed that microRNA-34a (miR-34a) functioned as a vital tumor suppressor in tumorigenesis and progression. However, the role and precise mechanisms of miR-34a and its regulatory gene network in initiation and progression of lung cancer in Gejiu and Xuanwei County, Yunnan Province, have not been elucidated. In the current study, we first found that miR-34a was downregulated in Gejiu lung squamous carcinoma YTMLC-90, Xuanwei lung adenocarcinoma XWLC-05, and other non-small cell lung carcinoma (NSCLC) cell lines, and miR-34a overexpression inhibited cell proliferation, migration and invasion, as well as induced cell apoptosis in YTMLC-90 and XWLC-05 cells. Our findings revealed that miR-34a is critical and cannot be considered as the area-specific non-coding RNA in initiation and progression of lung cancer in Gejiu and Xuanwei County. Next we revealed that miR-34a overexpression suppressed lung cancer growth and metastasis partially via increasing PTEN but reducing CDK6 expression that might lead to subsequent inactivation of PI3K/AKT pathway. Furthermore, our findings demonstrated that YY1 functioned as a tumor suppressor gene in initiation and progression of lung cancer in Gejiu and Xuanwei County. In conclusion, our findings in the study confirmed that miR-34a overexpression could simultaneously suppress tumor growth and metastasis and play a vital role in tumorigenesis and progression of NSCLC via increasing PTEN and YY1 expression, but decreasing CDK6. Most interestingly, our findings also raised doubts about the current ideas about these area-specific diseases.

scholarly journals Long non-coding RNA FENDRR inhibits migration and invasion of cutaneous malignant melanoma cells

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Xu-e Chen ◽  
Pu Chen ◽  
Shanshan Chen ◽  
Jin Lu ◽  
Ting Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Malignant Melanoma ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Related Factors ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Matrix Metallopeptidase ◽  
Long Non Coding Rna ◽  
A375 Cells

Abstract The present study aimed to investigate the effects of lncRNA FENDRR on the migration and invasion of malignant melanoma (MM) cells. The expression levels of FENDRR in MM tissues and MM cell lines were detected using qRT-PCR, followed by construction of FENDRR-knocked down and overexpressed stable cells. Then the effects of FENDRR on cell proliferation, migration and invasion were detected using MTT assay and Transwell assay. The protein expression levels of matrix metallopeptidase 2 (MMP2), MMP9, and related factors in JNK/c-Jun pathway were detected using Western blot. FENDRR was down-regulated in MM tissues and cell lines. Besides, its expression levels in different MM cells were diverse. Knockdown of FENDRR facilitated MM cells proliferation, migration and invasion in A375 cells, while overexpressing FENDRR had reverse results. In addition, MMPs and JNK/c-Jun pathway involved in the FENDRR-mediated regulation of MM cell proliferation, migration and invasion. Our results demonstrated that FENDRR mediated the metastasis phenotype of MM cells by inhibiting the expressions of MMP2 and MMP9 and antagonizing the JNK/c-Jun pathway.

scholarly journals RNA m1A Methyltransferase TRMT6 Predicts Poorer Prognosis and Promotes Malignant Behavior in Glioma

2021 ◽  
Vol 8 ◽  
Author(s):  
Beibei Wang ◽  
Lihua Niu ◽  
Zhengyang Wang ◽  
Zhihua Zhao
Keyword(s):  
Prognostic Value ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Cox Regression ◽  
Ectopic Expression ◽  
Malignant Progression ◽  
Migration And Invasion ◽  
Central Nervous System Tumor ◽  
Tumorigenesis And Progression ◽  
Public Datasets

Background: Glioma is the most prevalent central nervous system tumor in humans, and its prognosis remains unsatisfactory due to a lack of effective therapeutic targets. The ectopic expression of N1-methyladenosine (m1A) regulators is a key participant in tumorigenesis and progression. However, the m1A regulator expression status, prognostic value, and relationship with tumor clinical features in glioma remain unclear.Methods: Public datasets were used to analyze the mRNA and protein expression levels of m1A regulators. Kaplan–Meier and Cox regression analyses were performed to confirm the prognostic value of m1A regulators in glioma. Cellular experiments were conducted to verify the effect of TRMT6 on cell function. A comprehensive bioinformatics analysis was conducted to identify the potential molecular mechanisms regulated by TEMT6 in glioma.Results: We found that the dysregulation of m1A regulators was closely associated with tumorigenesis and progression in glioma. Furthermore, TRMT6 might be a powerful and independent biomarker for prognosis in glioma. Our study showed that inhibition of TRMT6 suppressed the proliferation, migration, and invasion of glioma cells. Mechanistically, TRMT6 may be involved in glioma progression by regulating cell cycle, PI3K-AKT, TGF-beta, MTORC1, NOTCH, and MYC pathways.Conclusions: Variation in m1A regulators was closely associated with malignant progression in glioma. Silencing TRMT6 suppressed the cell proliferation, migration, and invasion in glioma. m1A regulators, especially TRMT6, might play an essential role in the malignant progression of glioma.

scholarly journals LncRNA NEAT1 promotes endometrial cancer cell proliferation, migration and invasion by regulating the miR-144-3p/EZH2 axis

2019 ◽  
Vol 53 (4) ◽  
pp. 434-442 ◽  
Author(s):  
Wei Wang ◽  
Liang Ge ◽  
Xiao-Juan Xu ◽  
Ting Yang ◽  
Yue Yuan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Ishikawa Cells ◽  
Ec Cells ◽  
Proliferation And Invasion

Abstract Background Endometrial cancer (EC) is one of the most common gynaecological tumours in the worldwide. Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion in EC cells. However, the molecular mechanisms of NEAT1 in EC have not been fully clarified. We conducted this study to reveal the function of NEAT1 in EC tissues and cell lines. Materials and methods Cancer and adjacent tissues were collected from EC patients. HEC-1A and Ishikawa cells were cultured in vitro. NEAT1 expression was downregulated by transfecting small hairpin RNA (shRNA) and miR-144-3p was overexpressed by transfecting miR-144-3p mimics. Cell proliferation was detected by MTT assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assay. A dual-luciferase reporter assay was used to verify the relationship among NEAT1, EZH2, and miR-144-3p. The expression level of EZH2 was measured by Western blot and qPCR. Results NEAT1 was highly expressed in EC tissues and cells. Knockdown of NEAT1 inhibited the proliferation, migration and invasion of EC cells. Additionally, NEAT1 acted as a ceRNA of miR-144-3p, leading to EZH2 upregulation. Overexpression of miR-144-3p suppressed the proliferation and invasion of EC cells. Conclusions NEAT1 promotes EC cells proliferation and invasion by regulating the miR-144-3p/EZH2 axis.

scholarly journals LOXL1 modulates the malignant progression of colorectal cancer by inhibiting the transcriptional activity of YAP

2020 ◽  
Author(s):  
Lin Hu ◽  
Jing Wang ◽  
Yunliang Wang ◽  
Linpeng Wu ◽  
Chao Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Colony Formation ◽  
Transcriptional Activity ◽  
Tumour Growth ◽  
Molecular Mechanisms ◽  
Malignant Progression ◽  
Migration And Invasion

Abstract Background LOX-like 1 (LOXL1), as a lysyl oxidase, emerging evidences revealed the effect in cancer malignant progression. However, its role in colorectal cancer (CRC) and the underlying molecular mechanisms have not yet been elucidated. Methods LOXL1 expression in colorectal cancer was detected by immunohistochemistry, western blot and real-time PCR. In vitro , colony formation assay, wound healing assay, migration and invasion experiment were performed to investigate the effects of LOXL1 in cell proliferation, migration and invasion, respectively. In vivo , metastasis models and mouse xenograft were used to determine tumorigenicity and metastasis ability. Molecular biology experiments were utilized to reveal the underlying mechanisms of LOXL1 modulating Hippo pathway. Results LOXL1 is highly expressed in normal colon tissues compared with cancer tissues. In vitro, Silencing LOXL1 in CRC cell lines dramatically enhanced migration, invasion, and colony formation, while overexpression of LOXL1 manifested the opposite effects. Results of the in vivo experiments demonstrated that the enforced expression of LOXL1 in CRC cell lines had drastically inhibited the progression of metastasis and tumour growth. Mechanistically, LOXL1 inhibited the transcriptional activity of Yes-associated protein (YAP) was through interaction with MST1/2 and increasing the phosphorylation of MST1/2. Conclusions LOXL1 may function as an important tumour suppressor in regulating tumour growth, invasion and metastasis via negative regulating of YAP activity.

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