Mcgeeray5749
Furthermore, ZFP36 was manifested as the target gene of miR-513a-5p and negatively modulated by ADAMTS9-AS1. In addition, overexpression of ADAMTS9-AS1 neutralized the promoting impact of miR-513a-5p on the aggressiveness of breast cancer cells.
In conclusion, lncRNA ADAMTS9-AS1 inhibited the aggressive phenotypes of breast carcinoma cells via sponging miR-513a-5p and regulating ZFP36.
In conclusion, lncRNA ADAMTS9-AS1 inhibited the aggressive phenotypes of breast carcinoma cells via sponging miR-513a-5p and regulating ZFP36.
The dysregulated circular RNAs (circRNAs) are relevant to lung adenocarcinoma development. Nevertheless, the function and mechanism of hsa_circ_0020850 (circ_0020850) in lung adenocarcinoma development are uncertain.
A total of 35 lung adenocarcinoma patients were recruited, and the tumor and normal tissue samples were harvested. A549 and PC-9 cells were exhibited for the experiments in vitro. circ_0020850, microRNA-195-5p (miR-195-5p) and insulin receptor substrate 2 (IRS2) abundances were detected via quantitative reverse transcription-polymerase chain reaction or Western blot. Cell proliferation, apoptosis, migration and invasion were measured via cell counting kit-8 (CCK8) assay, colony formation, flow cytometry, transwell and Western blot. The relationship between miR-195-5p and circ_0020850 or IRS2 was tested via dual-luciferase reporter analysis. The function of circ_0020850 on cell growth in vivo was measured via xenograft model.
circ_0020850 expression was enhanced in lung adenocarcinoma tissues and cells. circ_0020850 silence suppressed cell proliferation, migration and invasion and facilitated apoptosis. click here miR-195-5p was targeted via circ_0020850, and its knockdown reversed the inhibitive effect of circ_0020850 silence on lung adenocarcinoma development. IRS2 was targeted via miR-195-5p, and miR-195-5p inhibited cell proliferation, migration and invasion and induced apoptosis via decreasing IRS2. circ_0020850 knockdown decreased IRS2 expression via regulating miR-195-5p. circ_0020850 down-regulation decreased lung adenocarcinoma xenograft tumor growth.
circ_0020850 knockdown repressed lung adenocarcinoma cell proliferation, migration and invasion and promoted apoptosis via regulating miR-195-5p and IRS2.
circ_0020850 knockdown repressed lung adenocarcinoma cell proliferation, migration and invasion and promoted apoptosis via regulating miR-195-5p and IRS2.
In order to investigate the role of miR-15b-5b in the progression of prostate cancer.
We employed RT-qPCR assay to analyze the transcriptional level of miR-15b-5b in cell lines including PC-3, prostate cancer tissues as well as normal prostate tissues. link2 The protein level of large tumor suppressor factor 2 (LATS2) was detected by Western blot in similar specimens. Bioinformatic analysis was used to predict the targets of miR-15b-5p, and dual-luciferase assay was performed to confirm the relationship of miR-15b-5p with LATS2. Cell proliferation assay and colony formation assay were used to assess the effects of miR-15b-5b on the proliferation of PC-3 cells. Multivariate analysis was performed to identify factors associated with overall survival using the Cox proportional hazards model.
MiR-15b-5b was up-regulated in prostate cancer tissues as well as cell lines, and increased expression of miR-15b-5b was highly correlated with the poor prognosis of patients with prostate cancer. Ectopic expression of miR-15b-5b promoted the proliferation of PC-3 cells. Reciprocally, silence of miR-15b-5b elicited opposite effects on cell proliferation. Mechanistically, we identified LATS2 as the target of miR-15b-5b, which in turn limited LATS2 expression in PC-3 cells. Furthermore, the stimulatory effects of miR-15b-5b on cell proliferation can be attenuated by overexpression of LATS2. Conversely, inhibition of LATS2 promoted the proliferation of PC-3 cells induced by miR-15b-5b. link3 Our data thus demonstrate that dysregulation of miR-15b-5b exacerbates prostate cancer progression via suppression of LATS2.
The identification of the oncogenic role of miR-15b-5b in prostate cancer thus proposes that miR-15b-5p might be a new therapeutic target for the treatment of prostate cancer.
The identification of the oncogenic role of miR-15b-5b in prostate cancer thus proposes that miR-15b-5p might be a new therapeutic target for the treatment of prostate cancer.
Esophageal squamous cell carcinoma (ESCC) persists among the most prevalent cancers worldwide. Angiogenesis represents a crucial element necessitated for tumor growth and metastasis in ESCC. In this study, we aimed to study the effect of microRNA (miR)-21 on angiogenesis in ESCC and its underlying mechanism.
Initially, the expression patterns of miR-21, SPRY1, and VEGF were determined in ESCC tissues and cells. The relationship between miR-21 and SPRY1 was identified using dual-luciferase reporter assay. Exosomes were subsequently isolated from the ESCC cells, followed by co-culture with the human umbilical venous endothelial cells (HUVECs). HUVEC proliferation and angiogenesis were determined by means of CCK-8, colony formation, and microtubule formation in vitro. Chicken chorioallantoic membrane (CAM) model and mouse xenograft model of ESCC cells were established to substantiate the function of miR-21 corresponding to the angiogenesis and tumor growth of ESCC, followed by microvascular density (MVD) evaluation.
Expression patterns of miR-21 and VEGF were elevated, while the SPRY1 expression pattern was repressed in ESCC tissues and cells. The downregulation of miR-21 and exosome-derived miR-21 impeded the proliferation and angiogenesis in HUVECs. Our data revealed that miR-21 could negatively target SPRY1, and positively target VEGF. The downregulation of miR-21 could evidently encumber the angiogenesis and tumor growth of ESCC in vivo, as evidenced by the decrease in number of branches of the microvessels and MVD.
Collectively, ESCC cell-derived exosome containing miR-21 promotes the proliferation and angiogenesis of HUVECs via SPRY1 downregulation and VEGF upregulation.
Collectively, ESCC cell-derived exosome containing miR-21 promotes the proliferation and angiogenesis of HUVECs via SPRY1 downregulation and VEGF upregulation.
Nasopharyngeal carcinoma (NPC) is among the most common malignancies derived from the epithelium of the nasopharynx. To date, the regulatory networks involved in NPC have not been fully identified. Previous studies revealed multiple loss-of-function mutations in NPC and specifically in cylindromatosis lysine 63 deubiquitinase (
); however, the exact role of CYLD in NPC progression and its potential mechanism remains unclear.
We performed immunohistochemical (IHC) staining and real-time quantitative polymerase chain reaction (qPCR) to measure
expression in NPC tissues, and Western blot was conducted to determine CYLD levels in NPC cell lines. Cell proliferation was detected by CCK8 assay and colony formation analysis, and apoptosis was determined by Annexin V/propidium iodide staining. Potential targets of CYLD were verified by co-immunoprecipitation and mass spectrometry. Xenograft assay was conducted to confirm the role of
in vivo.
We found that CYLD levels were significantly decreased in both NPC tissues and cell lines, and that
overexpression inhibited NPC cell proliferation and promoted apoptosis. Additionally, we revealed that CYLD bound and upregulated N-Myc downstream regulated 1 (NDRG1), and that silencing
abolished the tumor-suppressor effect of CYLD on NPC cells. Furthermore, CYLD suppressed tumor growth in xenograft mice models.
These results suggest CYLD as a tumor suppressor, potential biomarker for diagnosing NPC, and therapeutic target.
These results suggest CYLD as a tumor suppressor, potential biomarker for diagnosing NPC, and therapeutic target.
Many large-sample prospective randomized clinical trials investigating advanced gastric cancer (AGC) have confirmed the survival advantages of first-line, second-line, or third-line chemotherapy compared with their respective control groups. However, due to the ethical concerns of prospective clinical trials, it is impossible to conduct a randomized comparative study of patients who do not receive chemotherapy and those who receive a second-line or above chemotherapy. Few research reports have addressed the relationship between the number of chemotherapy lines and overall survival (OS) in patients with AGC. In the present study, we analyzed the impact of the number of chemotherapy lines on OS in AGC patients using real-world data.
This study collected the medical records of patients with AGC diagnosed at Shandong Cancer Hospital from December 2007 to December 2017. According to the treatment received, AGC patients were divided into groups that did not receive chemotherapy, those who received only 1 line, ements the results of prospective clinical trials that cannot be completed due to the ethical implications.The prognosis of HER2-positive metastatic breast cancer (MBC) has radically changed in recent years and continues to improve due to the broad application of effective therapies like monoclonal antibodies and small molecules targeting HER2. Persistent dependency of tumor cells on the oncogene HER2, on one hand, as well as low expression levels in healthy tissue, on the other hand, make this protein an ideal target for anti-cancer therapy. New HER2 targeting strategies including targeted delivery of cytotoxic drugs via HER2 receptor have been developed. Recently, the US Food and Drug Administration (FDA) approved three new drugs for the treatment of HER2-positive MBC the antibody-drug conjugate trastuzumab deruxtecan and the two tyrosine kinase inhibitors neratinib and tucatinib. Here, we summarize recent publications and developments of novel anti-HER2 therapies like monoclonal antibodies with improved properties compared to trastuzumab and bispecific antibodies, which bind two different HER-epitopes or bring T cells closer to tumor cells. Furthermore, novel antibody-drug conjugates and small molecules against HER2 are discussed. These developments coupled with new combination strategies (eg, with CDK4/6 inhibitors or immunotherapy) will change the treatment landscape for patients with HER2-positive MBC very soon and will hopefully further improve clinical outcomes.
To identify MRI-based radiomics signature (Rad-score) as a biomarker of risk stratification for disease-free survival (DFS) in patients with HER2-positive invasive breast cancer treated with trastuzumab-based neoadjuvant chemotherapy (NAC) and establish a radiomics-clinicoradiologic-based nomogram that combines Rad-score, MRI findings, and clinicopathological variables for DFS estimation.
A total of 127 patients were divided into a training set and testing set according to the ratio of 73. Radiomic features were extracted from multiphase CE-MRI (CE
). Rad-score was calculated using the LASSO (least absolute shrinkage and selection operator) regression analysis. The cutoff point of Rad-score to divide the patients into high- and low-risk groups was determined by receiver operating characteristic curve analysis. A Kaplan-Meier survival curves and the Log rank test were used to investigate the association of the Rad-score with DFS. Univariate and multivariate Cox proportional hazards model were used to determine the association of Rad-score, MRI features, and clinicopathological variables with DFS.
