• Extracellular vesicles
• Lung adenocarcinoma
• MicroRNA-130a-3p
• Osimertinib resistance
• Runt-related transcription factor 3

• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Drug Resistance, Neoplasm/genetics
• Aniline Compounds/pharmacology
• Adenocarcinoma of Lung/genetics
• Adenocarcinoma of Lung/drug therapy
• Adenocarcinoma of Lung/pathology
• Adenocarcinoma of Lung/metabolism
• Lung Neoplasms/drug therapy
• Lung Neoplasms/genetics
• Lung Neoplasms/pathology
• Lung Neoplasms/metabolism
• Cell Line, Tumor
• Acrylamides/pharmacology
• Acrylamides/therapeutic use
• Gene Expression Regulation, Neoplastic/drug effects
• Female
• Male
• Apoptosis/drug effects
• Middle Aged
• Aged
• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/therapeutic use
• Indoles
• Pyrimidines

• JSPS KAKENHI Japan Society for the Promotion of Science
• The Research Foundation for Pharmaceutical Sciences

• cervical cancer
• miRNAs
• oncogenic mirnas
• signalling pathway
• tumour suppressor

• Biomarker
• Cervical cancer
• Ovarian cancer
• Therapeutics
• miR-9

• Telocytes
• cancer
• microRNA
• microenvironment
• remodeling
• stem cells

• Telocytes
• Signal Transduction
• Stem Cells
• MicroRNAs
• Cell Differentiation

• EMT
• biomarker
• gastrointestinal tumors
• metastasis
• miRNA
• nutraceuticals
• tumor cell migration
• tumor microenvironment

• PNC0000001 Ministero della Salute, Piano Nazionale Complementare "D3 4 Health - Digital Driven Diagnostics, prognostics and therapeutics for sustainable Health care.
• RM12117A7F986146 Progetto Ateneo Sapienza 2021
• E85F22000060006 Ministero dell'Università e della Ricerca, PRIN 2020

• Diagnostic biomarker
• Salivary adenoid cystic carcinoma
• Therapeutic target
• miRNA

The combination of trastuzumab plus pertuzumab plus docetaxel as a first-line therapy in patients with HER2-positive metastatic breast cancer has provided significant clinical benefits compared to trastuzumab plus docetaxel alone. However, despite the therapeutic success of existing therapies targeting HER2, tumours invariably relapse. Therefore, there is an urgent need to improve our understanding of the mechanisms governing resistance, so that specific therapeutic strategies can be developed to provide improved efficacy. It is well known that the tumour microenvironment (TME) has a significant impact on cancer behaviour. Cancer-associated fibroblasts (CAFs) are essential components of the tumour stroma that have been linked to acquired therapeutic resistance and poor prognosis in breast cancer. For this reason, it would be of interest to identify novel biomarkers in the tumour stroma that could emerge as therapeutic targets for the modulation of resistant phenotypes. Conditioned medium experiments carried out in our laboratory with CAFs derived from HER2-positive patients showed a significant capacity to promote resistance to trastuzumab plus pertuzumab therapies in two HER2-positive breast cancer cell lines (BCCLs), even in the presence of docetaxel. In order to elucidate the components of the CAF-conditioned medium that may be relevant in the promotion of BCCL resistance, we implemented a multiomics strategy to identify cytokines, transcription factors, kinases and miRNAs in the secretome that have specific targets in cancer cells. The combination of cytokine arrays, label-free LC-MS/MS quantification and miRNA analysis to explore the secretome of CAFs under treatment conditions revealed several up- and downregulated candidates. We discuss the potential role of some of the most interesting candidates in generating resistance in HER2-positive breast cancer.

• CEA
• Tumor marker
• antigen
• diagnostic value
• miRNA
• prognostic value

Exosomal microRNAs (miRNAs) are considered as potential stable biomarkers in many types of human cancer, but investigations of plasma-derived exosomal miRNAs in oral squamous cell carcinoma (OSCC) are still lacking. The aim of this study is to evaluate the diagnostic and prognostic values of exosomal miR-130a in OSCC patients. Exosomes were isolated from plasma samples which were collected from 184 OSCC patients before surgery and 196 healthy individuals. Primary OSCC and paired adjacent noncancerous tissues were also obtained from 47 OSCC patients. The expression levels of miR-130a were analyzed by quantitative real-time PCR (qRT-PCR). Our results showed that the expression levels of exosomal miR-130a were significantly higher in OSCC patients than those of the healthy controls (p < 0.0001). Also, the expression of miR-130a was also significantly upregulated in OSCC tissues compared with paired adjacent noncancerous tissues (p < 0.0001). A significant positive correlation was found between exosomal miR-130a and tissue miR-130a levels. Receiver operating characteristic (ROC) analyses yielded an AUC value of 0.812 in discriminating OSCC patients from healthy controls. Furthermore, high levels of exosomal miR-130a were associated with the late T-stage (p=0.024), advanced TNM stage (p=0.003), and poorly differentiated OSCC (p=0.013). Patients with high exosomal miR-130a expression had significantly worse 3-year overall survival (OS) and recurrence-free survival (RFS). Multivariate analysis indicated that exosomal miR-130a was an independent prognostic factor for OS (p=0.001) and RFS (p=0.003). Our results suggest that exosomal miR-130a may serve as a promising diagnostic and prognostic biomarker for OSCC patients.

Aberrant activation of the PI3K/AKT/mTOR pathway is attributed to the pathogenesis of oral squamous cell carcinoma (OSCC). In recent years, increasing evidence suggests the involvement of microRNAs (miRNAs) in oral carcinogenesis by acting as tumor suppressors or oncogenes. TSC1, as a component of the above pathway, regulates several cellular functions such as cell proliferation, apoptosis, migration and invasion. Downregulation of TSC1 is reported in oral as well as several other cancers and is associated with an unfavourable clinical outcome in patients. Here we show that oncogenic miR-130a binds to the 3′UTR of TSC1 and represses its expression. MiR-130a-mediated repression of TSC1 increases cell proliferation, anchorage independent growth and invasion of OSCC cells, which is dependent on the presence of the 3′UTR in TSC1. We observe an inverse correlation between the expression levels of miR-130a and TSC1 in OSCC samples, suggesting that their interaction is physiologically relevant. Delivery of antagomiR-130a to OSCC cells results in a significant decrease in xenograft size. Taken together, the findings of the study indicate that miR-130a-mediated TSC1 downregulation is not only a novel mechanism in OSCC, but also the restoration of TSC1 levels by antagomiR-130a may be a potential therapeutic strategy for the treatment of OSCC.

• ATG16L1
• Crohn’s disease
• NF-κB pathway
• colitis
• miR-130a-3p

Cervical cancer is the most common gynecological cancer in women worldwide. Human papillomavirus (HPV) is required but not sufficient for developing cervical cancer. HPV E6 and E7 proteins are able to directly interact with certain nuclear receptors; however, whether steroid hormone receptors mediate cervical carcinogenesis is not completely understood. The present study demonstrated via immunohistochemistry that estrogen receptor α (ERα) and androgen receptor (AR) expression were decreased in a sequential manner from healthy cervical tissues to cervical intraepithelial neoplasia tissues and further to cervical cancer (CC) tissues, whereas microRNA (miR)-130a-3p expression levels were higher in CC tissues compared with healthy tissues. Both ERα and AR were direct targets of miR-130a-3p, as determined by performing luciferase reporter assays and western blotting. Functionally, compared with the corresponding control groups, miR-130a-3p knockdown, ERα overexpression and AR overexpression significantly inhibited CC cell proliferation and invasion, as demonstrated by the results obtained from the Cell Counting Kit-8 and Transwell assays in vitro. In addition, antagomiR-130a decreased tumor size and weight in vivo compared with control antagomiR as determined via the xenograft tumor growth assay. Therefore, the results suggested that miR-130a-3p might contribute to tumor progression by suppressing ERα and AR, and serve as a promising candidate target for the treatment of patients with CC.

• androgen receptor
• cervical cancer
• estrogen receptor α
• invasion
• microRNA
• neoplasm

• ATG2B
• arteriosclerosis obliterans
• autophagy
• microRNA-130a
• vascular smooth muscle cells

• bortezomib
• efficacy
• miR-181a-5p
• miR-215-5p
• miR-376c-3p
• microRNA
• multiple myeloma
• refractory
• resistance
• sensitivity

Primary gastrointestinal diffuse large B-cell lymphoma (PGI-DLBCL) is a highly heterogeneous type of non-Hodgkin lymphoma. A number of studies have demonstrated that microRNA-130a (miR-130a) serves a role in the tumorigenesis and prognosis of numerous human tumors. However, to the best of our knowledge, the prognostic significance of miR-130a in PGI-DLBCL remains unknown. The present study explored the association between miR-130a and the clinical outcomes of PGI-DLBCL. Relative miR-130a expression was assessed by reverse transcription-quantitative PCR. Immunohistochemistry was used to detect expression levels of BCL-2, c-MYC, neprilysin, B-cell lymphoma 6 protein, PWWP domain-containing DNA repair factor 3A and proliferation marker protein Ki-67. A receiver operating characteristic curve was constructed to analyze the specificity and sensitivity of microRNA levels in the diagnosis of PGI-DLBCL. Survival curves were constructed using the Kaplan-Meier method. In the present study, miR-130a expression was notably higher in patients with PGI-DLBCL compared with in the controls (P<0.0001). miR-130a overexpression was closely associated with a high International Prognostic Index score (3–5) and drug resistance (P=0.017 and P=0.044, respectively). No significant difference in other clinical features was observed. Patients with increased expression levels of miR-130a had lower overall survival [hazard ratio (HR), 2.998; 95% CI, 1.347-6.673; P=0.007] and progression-free survival (HR, 3.325; 95% CI, 1.488-7.429; P=0.003) compared with patients who had lower expression levels of miR-130a. Furthermore, multivariate Cox regression analysis suggested that miR-130a was a negative prognostic parameter in PGI-DLBCL. Therefore, upregulation of miR-130a could become a potential prognostic marker for PGI-DLBCL. Additionally, further study of these results may have important guiding significance for the prognosis of patients with PGI-DLBCL in the clinical setting.

• expression
• microRNA-130a
• primary gastrointestinal diffuse large B-cell lymphoma
• prognosis
• resistance

• cell apoptosis
• cell growth
• clinicopathological characteristics
• diagnostic value
• microRNA-130a
• microRNA-203
• papillary thyroid carcinoma

Aging is associated with impaired neovascularization in response to ischemia. MicroRNAs are small noncoding RNAs emerging as key regulators of physiological and pathological processes. Here we investigated the potential role of microRNAs in endothelial cell senescence and age-dependent impairment of neovascularization. Next generation sequencing and qRT-PCR analyses identified miR-130a as a pro-angiogenic microRNA which expression is significantly reduced in old mouse aortic endothelial cells (ECs). Transfection of young ECs with a miR-130a inhibitor leads to accelerated senescence and reduced angiogenic functions. Conversely, forced expression of miR-130a in old ECs reduces senescence and improves angiogenesis. In a mouse model of hindlimb ischemia, intramuscular injection of miR-130a mimic in older mice restores blood flow recovery and vascular densities in ischemic muscles, improves mobility and reduces tissue damage. miR-130a directly targets antiangiogenic homeobox genes MEOX2 and HOXA5. MEOX2 and HOXA5 are significantly increased in the ischemic muscles of aging mice, but forced expression of miR-130a reduces the expression of these factors. miR-130a treatment after ischemia is also associated with increased number and improved functional activities of pro-angiogenic cells (PACs). Forced expression of miR-130a could constitute a novel strategy to improve blood flow recovery and reduce ischemia in older patients with ischemic vascular diseases.

• aging
• angiogenesis
• microRNA
• neovascularization
• senescence

Effect of micro ribonucleic acid (miR)-130a on neuronal apoptosis in rats with cerebral infarction (CI) was studied to explore whether phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) is involved in the regulation of neuronal apoptosis. Thirty-six Sprague-Dawley (SD) rats were randomly divided into blank control group, model group and miR-130a low-expression group. miR-130a was determined by quantitative polymerase chain reaction (qPCR), the content of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 was detected using the enzyme-linked immunosorbent assay (ELISA) kits, and the neuronal apoptosis level in each group was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The neurobehavioral score was significantly lower in model group than that in blank control group (P<0.01), while it was significantly higher in miR-130a low-expression group than that in model group (P<0.01). Compared with blank control group, the model group had obviously increased content of TNF-α and IL-6 (P<0.01), decreased content of IL-10 (P<0.01), more apoptotic neurons (P<0.01), higher expression of caspase-3 (P<0.01), and obviously lower Bcl-2/Bax (P<0.01). Moreover, expression of phosphorylated (p)-PTEN, PI3K and p-Akt in brain tissues was remarkably lower in the model group than those in the blank control group (P<0.01). The expression level of miR-130a in brain tissues of CI rats is significantly increased. miR-130a promotes the release of inflammatory factors and facilitates neuronal apoptosis through suppressing the PTEN/PI3K/Akt signaling pathway.

• PTEN/PI3K/Akt signaling pathway
• apoptosis
• cerebral infarction
• miR-130a

• Specificity protein 1
• TMZ resistance
• glioblastoma
• miR-130a-3p
• proliferation

• African Americans
• RNA
• epigenomics
• health care disparities
• long noncoding
• microRNAs
• pan-cancer

• Cancer
• Prognosis
• Systematic evaluation
• miRNA-130a
• miRNA-130b

• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/mortality
• Databases, Nucleic Acid
• Disease-Free Survival
• Female
• Humans
• Kaplan-Meier Estimate
• Liver Neoplasms/genetics
• Liver Neoplasms/metabolism
• Liver Neoplasms/mortality
• Male
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Neoplasms/genetics
• Neoplasms/metabolism
• Neoplasms/mortality
• Prognosis
• Progression-Free Survival
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/mortality
• Transcriptome
• Translational Research, Biomedical

• GEO
• Lung cancer
• TCGA
• bioinformatics
• methylation
• miR-130b

• Carcinoma, Squamous Cell/genetics
• Carcinoma, Squamous Cell/physiopathology
• Computational Biology/statistics & numerical data
• DNA Methylation/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• Lung Neoplasms/genetics
• Lung Neoplasms/physiopathology
• MicroRNAs/genetics

• Migration
• SPOCK1
• cigarette-smoke
• lung cancer
• miR-130a-3p

• Adenocarcinoma/metabolism
• Apoptosis
• Cell Line, Tumor
• Cell Movement
• Data Mining
• Down-Regulation
• Epithelial Cells/drug effects
• Gene Expression Regulation/drug effects
• Humans
• Lung Neoplasms/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Proteoglycans/genetics
• Proteoglycans/metabolism
• RNA, Small Interfering
• Respiratory Mucosa/cytology
• Smoke/adverse effects
• Transfection

Concerning adenocarcinomas of the esophagogastric junction, neoadjuvant chemotherapy is regularly implemented, but patients' response varies greatly, with some cases showing no therapeutic effect, being deemed as chemoresistant. Small, noncoding RNAs (miRNAs) have evolved as key players in biological processes, including malignant diseases, often promoting tumor growth and expansion. In addition, specific miRNAs have been implicated in the development of chemoresistance through evasion of apoptosis, cell cycle alterations, and drug target modification. We performed a retrospective study of 33 patients receiving neoadjuvant chemotherapy by measuring their miRNA expression profiles. Histologic tumor regression was evaluated using resection specimens, while miRNA profiles were prepared using preoperative biopsies without prior therapy. A preselected panel of 96 miRNAs, known to be of importance in various malignancies, was used to test for significant differences between responsive (chemosensitive) and nonresponsive (chemoresistant) cases. The cohort consisted of 12 nonresponsive and 21 responsive cases with the following 4 miRNAs differentially expressed between both the groups: hsa-let-7f-5p, hsa-miRNA-221-3p, hsa-miRNA-31-5p, and hsa-miRNA-191-5p. The former 3 showed upregulation in chemoresistant cases, while the latter showed upregulation in chemosensitive cases. In addition, significant correlation between high expression of hsa-miRNA-194-5p and prolonged survival could be demonstrated (p value <0.0001). In conclusion, we identified a panel of 3 miRNAs predicting chemoresistance and a single miRNA contributing to chemosensitivity. These miRNAs might function as prognostic biomarkers and enable clinicians to better predict the effect of one or more reliably select patients benefitting from (neoadjuvant) chemotherapy.

• CYLD
• Fibroblasts
• Hypertrophic scar
• microRNA-130a

• cardiac cancer
• cell apoptosis
• cell viability
• chemo-sensitivity
• lncRNA H19
• miR-130a-3p
• miR-17-5p
• radio-sensitivity

• Angiogenesis Inducing Agents/pharmacology
• Animals
• Biocompatible Materials/pharmacology
• Cells, Cultured
• Exosomes/metabolism
• Human Umbilical Vein Endothelial Cells
• Humans
• Lithium/pharmacology
• Mesenchymal Stem Cells/drug effects
• Mesenchymal Stem Cells/metabolism
• MicroRNAs/metabolism
• Neovascularization, Physiologic/drug effects
• Rats

miRNAs play a crucial role in cancer development and progression. However, results on the impact of miRNAs on drug sensitivity and tumor biology vary, and most studies to date focussed on either increasing or decreasing miRNA expression levels. Therefore, the current study investigated the role of different expression levels of miR-130a-3p and miR-148a-3p on drug resistance and tumor biology in four esophageal squamous cell carcinoma cell lines. Interestingly, up- and downregulation of both miRNAs significantly increased sensitivity towards chemotherapy. MiRNA modulation also reduced adherence and migration potential, and increased apoptosis rates. Target analyses showed that up- and downregulation of both miRNAs activated the apoptotic p53-pathway via increased expression of either BAX (miR-148a-3p) or Caspase 9 (miR-130a-3p). miR-148a-3p downregulation seemed to mediate its effects primarily via regulation of Bim rather than Bcl-2 levels, whereas we found the opposite scenario following miR-148a-3p upregulation. A similar effect was observed for miR-130a-3p regulating Bcl-2 and XIAP. Our data provide the first evidence that miRNA modulation in both directions may lead to similar effects on chemotherapy response and tumor biology in esophageal squamous cell carcinoma. Most interestingly, up- and downregulation seem to mediate their effects via modulating the balance of several validated or predicted targets.

• Cancer stem cell
• Gene-directed enzyme prodrug therapy
• Glioblastoma
• Glioma
• Intramedullary spinal cord tumor
• Recovery neurobiology
• Spinal cord astrocytoma
• Tumor survival cell

• Biomarker
• Molecular diagnostics
• Molecular therapy
• Pediatric otolaryngology
• miRNA
• microRNA

Non-invasive diagnostic biomarkers may contribute to an early identification of gastric cancer (GC) and improve the clinical management. Unfortunately, no sensitive and specific screening biomarkers are available yet and the currently available approaches are limited by the nature of the disease. GC is a heterogenic disease with various distinct genetic and epigenetic events that occur during the multifactorial cascade of carcinogenesis. MicroRNAs (miRNAs) are commonly deregulated in gastric mucosa during the Helicobacter pylori infection and in stepwise manner from chronic gastritis, through preneoplastic conditions such as atrophic gastritis and intestinal metaplasia, to early dysplasia and invasive cancer. Identification of miRNAs in blood in 2008 led to a great interest on miRNA-based diagnostic, prognostic biomarkers in GC. In this review, we provide the most recent systematic review on the existing studies related to miRNAs as diagnostic biomarkers for GC. Here, we systematically evaluate 75 studies related to differential expression of circulating miRNAs in GC patients and provide novel view on various heterogenic aspects of the existing data and summarize the methodological differences. Finally, we highlight several important aspects crucial to improve the future translational and clinical research in the field.

• MicroRNA
• Biomarkers
• Screening
• Stomach
• Gastric cancer
• Systematic review
• Blood
• Serum
• Plasma

• Biomarkers, Tumor/blood
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Carcinogenesis/genetics
• Circulating MicroRNA/blood
• Circulating MicroRNA/genetics
• Circulating MicroRNA/metabolism
• Early Detection of Cancer/methods
• Early Detection of Cancer/trends
• Gastric Mucosa/pathology
• Gene Expression Profiling
• Gene Expression Regulation, Neoplastic
• Helicobacter Infections/microbiology
• Helicobacter Infections/pathology
• Humans
• Precancerous Conditions/genetics
• Precancerous Conditions/pathology
• Stomach Neoplasms/blood
• Stomach Neoplasms/diagnosis
• Stomach Neoplasms/genetics

• TET1
• colorectal cancer
• miR-21
• proliferation

Background: Resistance towards chemotherapy is a major obstacle in the treatment of esophageal squamous cell carcinoma (ESCC). We investigated the role of specific microRNAs in chemotherapy resistance and tumor biology. Methods: We selected three microRNAs from characteristic microRNA signatures of resistant ESCC (hsa-miR-125a-5p, hsa-miR-130a-3p, hsa-miR-1226-3p), and hsa-miR-148a-3p. Effects on chemotherapy, adhesion, migration, apoptosis and cell cycle were assessed in six ESCC cell lines. Target analyses were performed using Western blotting and luciferase techniques. Results: MiR-130a-3p sensitized cells towards cisplatin in 100% of cell lines, miR-148a-3p in 83%, miR-125a-5p in 67%, miR-1226-3p in 50% (p ≤ 0.04). MiR-130a-3p sensitized 83% of cell lines towards 5-FU, miR-148a-3p/miR-125a-5p/miR-1226-3p only 33% (p ≤ 0.015). Several resistance-relevant pathways seem to be targeted on various levels. Bcl-2 was confirmed as a direct target of miR-130a-3p and miR-148a-3p, and p53 as a target of miR-125a-5p. All microRNAs decreased migration and adhesion, except miR-130a-3p, and increased apoptosis. Simultaneous manipulation of two microRNAs exhibited additive sensitizing effects towards cisplatin in 50% (miR-125a-5p/miR-148a-3p), and 75% (miR-148a-3p/miR-130a-3p) of cell lines (p ≤ 0.006). Conclusion: Our data present strong evidence that specific microRNA signatures are responsible for drug resistance and aggressiveness of ESCC. Final functional readout of these complex processes appears to be more important than single microRNA-target interactions.

• K270: KYSE-270
• K410: KYSE-410
• chemotherapy
• esophageal squamous cell carcinoma
• metastasis
• miR: miRNA
• microRNA
• resistance

• GATA4
• cyclooxygenase-2
• gastric cancer
• microRNA-144

• EMT
• TBL1XR1
• gastric cancer
• metastasis
• miR-130a-3p

Mounting evidence has indicated microRNA (miR) dysregulation and the Wnt/β-catenin signaling pathway jointly drive carcinogenesis, cancer metastasis, and drug-resistance. The current review will focus on the role of the crosstalk between miRs and the Wnt/β-catenin signaling pathway in cancer development. MiRs were found to activate or inhibit the canonical Wnt pathway at various steps. On the other hand, Wnt activation increases expression of miR by directly binding to its promoter and activating transcription. Moreover, there are mutual feedback loops between some miRs and the Wnt/β-catenin signaling pathway. Clinical trials of miR-based therapeutic agents are investigated for solid and hematological tumors, however, challenges concerning low bioavailability and possible side effects must be overcome before the final clinical application. This review will describe current understanding of miR crosstalk with the Wnt/β-catenin signaling cascade. Better understanding of the regulatory network will provide insight into miR-based therapeutic development.

• Wnt/β-catenin signaling pathway
• cancer
• microRNA

• Glioma
• HMGB2
• miR-130a

• gastric cancer
• meta-analysis
• microRNA
• prognosis

• CRMP4
• gastric cancer
• miR-130a
• microRNA-130a

• Cancer
• Drug resistance
• MiR-130a
• MicroRNA

• Antineoplastic Agents/therapeutic use
• Drug Resistance, Neoplasm/genetics
• Humans
• MicroRNAs/genetics
• Neoplasms/drug therapy
• Neoplasms/genetics
• Signal Transduction