Contrast-enhanced ultrasound-guided biopsy of suspicious breast lesions on contrast-enhanced mammography and contrast-enhanced MRI: a case series.

PURPOSE: To assess the effectiveness of contrast-enhanced ultrasound (CEUS) in guiding biopsies of breast lesions that were detected on contrast-enhanced mammography (CEM) or contrast-enhanced breast MRI (CE-MRI) but were not clearly visible on B-mode ultrasound (B-US). METHODS: In this study, 23 lesions in 16 patients were selected for CEUS-guided biopsy due to poor visualization on B-US despite being detected on CEM (n = 20) or CE-MRI (n = 3). B-US, color Doppler ultrasound (CDUS), and CEUS were used to visualize the suspicious lesions, followed by a CEUS-guided core needle biopsy using Sonazoid as the contrast agent. The accuracy of the biopsy was assessed based on pathology-radiology concordance and 12-month imaging follow-up. The conspicuity scores for lesion visualization were evaluated using a 5-point conspicuity scale agreed upon by two breast radiologists. RESULTS: The enhancing lesions detected on CEM/CE-MRI had an average size of 1.6 ± 1.3 cm and appeared as mass-enhancing (61%) or non-mass-enhancing (39%). The lesions had mean conspicuity scores of 2.30 on B-US, 2.78 on CDUS, and 4.61 on CEUS, with 96% of the lesions showing contrast enhancement on CEUS. CEUS-guided biopsy showed increased visibility in 96% and 91% of the lesions compared to B-US and CDUS, respectively. The overall accuracy of CEUS-guided biopsy was 100% based on concordance with histology and 12-month follow-up. CONCLUSIONS: CEUS enhances the visibility of suspicious CEM/CE-MRI lesions that are poorly visible on B-US during biopsy procedures.

Rapid identification and detection of aristolochic acids in the herbal extracts by Raman spectroscopy.

Herbs containing aristolochic acids (AAs) have already been proven to be highly carcinogenic and nephrotoxic. In this study, a novel surface-enhanced Raman scattering (SERS) identification method was developed. Ag-APS nanoparticles with a particle size of 3.53 ± 0.92 nm were produced by combining silver nitrate and 3-aminopropylsilatrane. The reaction between the carboxylic acid group of aristolochic acid I (AAI) and amine group of Ag-APS NPs was used to form amide bonds, and thus, concentrate AAI, rendering it easy to detect via SERS and amplified to obtain the best SERS enhancement effect. Detection limit was calculated to be approximately 40 nM. Using the SERS method, AAI was successfully detected in the samples of four Chinese herbal medicines containing AAI. Therefore, this method has a high potential to be applied in the future development of AAI analysis and rapid qualitative and quantitative analysis of AAI in dietary supplements and edible herbs.

BiTE-Secreting CAR-γδT as a Dual Targeting Strategy for the Treatment of Solid Tumors.

HLA-G is considered as an immune checkpoint protein and a tumor-associated antigen. In the previous work, it is reported that CAR-NK targeting of HLA-G can be used to treat certain solid tumors. However, the frequent co-expression of PD-L1 and HLA-G) and up-regulation of PD-L1 after adoptive immunotherapy may decrease the effectiveness of HLA-G-CAR. Therefore, simultaneous targeting of HLA-G and PD-L1 by multi-specific CAR could represent an appropriate solution. Furthermore, gamma-delta T (γδT) cells exhibit MHC-independent cytotoxicity against tumor cells and possess allogeneic potential. The utilization of nanobodies offers flexibility for CAR engineering and the ability to recognize novel epitopes. In this study, Vδ2 γδT cells are used as effector cells and electroporated with an mRNA-driven, nanobody-based HLA-G-CAR with a secreted PD-L1/CD3ε Bispecific T-cell engager (BiTE) construct (Nb-CAR.BiTE). Both in vivo and in vitro experiments reveal that the Nb-CAR.BiTE-γδT cells could effectively eliminate PD-L1 and/or HLA-G-positive solid tumors. The secreted PD-L1/CD3ε Nb-BiTE can not only redirect Nb-CAR-γδT but also recruit un-transduced bystander T cells against tumor cells expressing PD-L1, thereby enhancing the activity of Nb-CAR-γδT therapy. Furthermore, evidence is provided that Nb-CAR.BiTE redirectes γδT into tumor-implanted tissues and that the secreted Nb-BiTE is restricted to the tumor site without apparent toxicity.

Taiwan's National Health Insurance at the Emergency Department following the COVID-19 outbreak.

Taiwan's National Health Insurance (NHI) is a widely acclaimed universal healthcare system. In the past few years, particularly following the COVID-19 outbreak, challenges related to maintaining the NHI system have surfaced. Since 2020, NHI has faced a series of challenges, including excessive patient visits to the hospital emergency department, a lack of an effective primary care and referral system, and a high turnover rate of healthcare workers. We review major problems related to Taiwan's NHI, emphasizing input from frontline healthcare workers. We provide recommendations for potential policies addressing the concerns around NHI, for example, strengthening the role of primary care services under the NHI administration, reducing the high turnover rate of healthcare workers, and increase the premium and copayments. We hope that this policy analysis may allow policymakers and scholars to understand both the merits and critical problems related to NHI from the clinical perspective.

Imiquimod-induced ROS production causes lysosomal membrane permeabilization and activates caspase-8-mediated apoptosis in skin cancer cells.

BACKGROUND: Lysosomal cell death is induced by lysosomal membrane permeabilization (LMP) and the subsequent release of lysosomal proteolytic enzymes, including cathepsins (CTSs), which results in mitochondrial dysfunction and apoptosis. Imiquimod (IMQ), a synthetic TLR7 ligand, has both antiviral and antitumor activity against various skin malignancies in clinical treatment. Previously, we demonstrated IMQ not only caused lysosomal dysfunction but also triggered lysosome biogenesis to achieve lysosomal adaptation in cancer cells. OBJECTIVE: To determine whether lysosomes are involved in IMQ-induced apoptosis. METHODS: The human skin cancer cell lines BCC, A375 and mouse melanoma cell line B16F10 were used in all experiments. Cell death was determined by the Cell Counting Kit-8 (CCK-8) assay and DNA content assay. Protein expression was determined by immunoblotting. Caspase-8 activity was assessed using a fluorescence caspase-8 kit and determined by flow cytometry and confocal microscopy. RESULTS: IMQ not only induced lysosome damage but also abrogated lysosome function in skin cancer cells. IMQ-induced caspase-8 activation contributed to the processes of lysosomal cell death. Moreover, the use of ROS scavengers significantly abolished caspase-8 activation and inhibited IMQ-induced LMP. Additionally, pharmacological inhibition of CTSD not only abrogated caspase-8 activation but also rescued IMQ-induced cell death. Finally, lysosome-alkalizing agents enhanced the cytotoxicity of IMQ in vitro and in vivo. CONCLUSIONS: IMQ-induced ROS accumulation promotes LMP, releases CTSs into the cytosol, stimulates caspase-8 activation and finally causes lysosomal cell death. Lysosomal cell death and the CTSD/caspase-8 axis may play a crucial role in IMQ-induced cell death.

Quantum dot assisted precise and sensitive fluorescence-based formaldehyde detection in food samples.

Formaldehyde has an extremely reactive carbonyl group, commonly used as an antibacterial agent to sterilize and prevent food to spoil. This article describes an efficient and rapid detection method of formaldehyde from an aqueous solution by synthesizing 3-Aminopropyltriethoxysilane (APTES) quantum dots (Nano A) which react with formaldehyde to generate a Schiff base reaction. The photoinduced electron transfer produced by the quantum dots themselves results in fluorescence quenching to detect formaldehyde. The detection limit can reach 10-9 M, and it can further be used to detect formaldehyde content in foods, such as baby vegetables, mushrooms, and vermicelli among other daily foods.

Engineered mesoporous biochar derived from rice husk for efficient removal of malachite green from wastewaters.

Extremely soluble Malachite green (MG) acts as potential carcinogen for aquatic life in polluted aqueous environments. Current study aims to modify rice husk derived biochar to improve its removal efficiency for MG from MG-containing wastewaters. The hydrothermal alkali activation was effective for preparing modified biochar (RHMB) from native biochar (RHB) derived from rice husk. After modification, surface area and pore volume of RHMB was determined respectively 434.62 m2g-1 and 287.28 cm3g-1, significantly improved from native RHB values 21.764 m2g-1 and 65.53 cm3g-1. Pseudo second order kinetic model fitted well. RHMB exhibits an equilibrium adsorption capacity of 373.02 mg g-1. RHMB showed an excellent MG removal ability and was not susceptible to ion interference even at highly saline environments. It has exhibited 96.96 ± 1.17% removal efficiency of MG and is expected to be used as potential adsorbent for MG remediation from aquaculture wastewater and other MG containing industrial wastewaters.

Catalytic oxidation and deionization of nitrite and nitrate ions using mesoporous carbon-supported nano-flaky cobalt and nickel oxyhydroxides.

The composite electrode of NiCo oxide supported by porous carbon was synthesized for nitrite oxidation and nitrate electro-sorption. The crystal structure and chemical state of the Co and Ni oxyhydroxides which were precipitated on loofah-derived activated carbon (AC) using hypochlorite were characterized by X-ray diffraction (XRD), scanning electron microscope (SEM), X-ray photoelectron spectroscopy (XPS), and BET surface area. The voltammetry showed that the redox couple of Co(II)/Co(III) and Ni(II)/Ni(III) as the mediator catalytically transferred the electrons of NO2-/NO3-; the Ni site had a relatively high transfer coefficient and diffusive current, while the Co site was better in the capacitive removal of the nitrite and nitrate compounds. A batch electrolysis of nitrite ions was operated under constant anodic potential mode (0 to + 1.5 V vs. Ag/AgCl) to assess the performance of the composite electrodes. The adsorption capacity of NiCo/AC (Ni = 5% and Co = 5% on AC by weight) was 23.5 mg-N g-1, which was twice that of AC substrate (7.5 mg-N g-1), based on a multilayer adsorption model. The steady-state kinetics of the consecutive reaction were derived to determine the rate steps of the electrochemical oxidation of NO2- and adsorption of NO3-.

CaO recovered from eggshell waste as a potential adsorbent for greenhouse gas CO2.

The growing number of industrial carbon emissions have resulted in a significant increase in the greenhouse gas carbon dioxide (CO2), which, in turn, will have a major impact on climate change. Therefore, the reduction, storage, and reuse of CO2 is an important concern in modern society. Calcium oxide (CaO) is known to be an excellent adsorbent of CO2 in a high-temperature environment. However, since deterioration of the adsorbent is likely to occur after repeated cycles of adsorption under high temperature conditions, it would be desirable to mitigate this phenomenon, in order to maintain the stability of CaO. In the present study, common eggshell waste was used as the starting material. The main component of eggshell waste is calcium carbonate (CaCO3), which was purified to produce CaO. Different surfactants and amino-containing polymers were added to synthesize CaO-based adsorbents with different configurations and pore sizes. The amount of CO2 adsorbed was determined using a thermogravimetric analyzer (TGA). The results showed that the CO2 adsorption capacity of the synthetic CaO recovered from purified eggshell waste could reach 0.6 g-CO2/g-sorbent, indicating a good adsorption capacity. CaO modified with a dopamine-containing polymer was shown to have an adsorption capacity of 0.62 g-CO2/g-sorbent. Moreover, it showed an excellent adsorption capacity of 0.40 g-CO2/g-sorbent, even after 10 cycles of CO2 adsorption. The present study suggests that using eggshell waste to synthesize CaO-based adsorbents for effective CO2 adsorption can not only reduce environmental waste, but also have the potential to capture greenhouse gas CO2 emissions, which conforms to the principles of green chemistry.

Utilizing Edible Agar as a Carrier for Dual Functional Doxorubicin-Fe3O4 Nanotherapy Drugs.

The purpose of this study was to use agar as a multifunctional encapsulating material to allow drug and ferromagnetism to be jointly delivered in one nanoparticle. We successfully encapsulated both Fe3O4 and doxorubicin (DOX) with agar as the drug carrier to obtain DOX-Fe3O4@agar. The iron oxide nanoparticles encapsulated in the carrier maintained good saturation of magnetization (41.9 emu/g) and had superparamagnetism. The heating capacity test showed that the specific absorption rate (SAR) value was 18.9 ± 0.5 W/g, indicating that the ferromagnetic nanoparticles encapsulated in the gel still maintained good heating capacity. Moreover, the magnetocaloric temperature could reach 43 °C in a short period of five minutes. In addition, DOX-Fe3O4@agar reached a maximum release rate of 85% ± 3% in 56 min under a neutral pH 7.0 to simulate the intestinal environment. We found using fluorescent microscopy that DOX entered HT-29 human colon cancer cells and reduced cell viability by 66%. When hyperthermia was induced with an auxiliary external magnetic field, cancer cells could be further killed, with a viability of only 15.4%. These results show that agar is an efficient multiple-drug carrier, and allows controlled drug release. Thus, this synergic treatment has potential application value for biopharmaceutical carrier materials.

Surface Modified ß-Tricalcium phosphate enhanced stem cell osteogenic differentiation in vitro and bone regeneration in vivo.

A major number of studies have demonstrated Beta-tricalcium phosphate (ß-TCP) biocompatibility, bioactivity, and osteoconductivity characteristics in bone regeneration. The aim of this research was to enhance ß-TCP's biocompatibility, and evaluate its physicochemical properties by argon glow discharge plasma (GDP) plasma surface treatment without modifying its surface. Treated ß-TCP was analyzed by scanning electron microscopy (SEM), energy-dispersive spectrometry, X-ray photoelectron spectroscopy (XPS), X-ray diffraction analysis, and Fourier transform infrared spectroscopy characterization. To evaluate treated ß-TCP biocompatibility and osteoblastic differentiation, water-soluble tetrazolium salts-1 (WST-1), immunofluorescence, alkaline phosphatase (ALP) assay, and quantitative real-time polymerase chain reaction (QPCR) were done using human mesenchymal stem cells (hMSCs). The results indicated a slight enhancement of the ß-TCP by GDP sputtering, which resulted in a higher Ca/P ratio (2.05) than the control. Furthermore, when compared with control ß-TCP, we observed an improvement of WST-1 on all days (p < 0.05) as well as of ALP activity (day 7, p < 0.05), with up-regulation of ALP, osteocalcin, and Osteoprotegerin osteogenic genes in cells cultured with the treated ß-TCP. XPS and SEM results indicated that treated ß-TCP's surface was not modified. In vivo, micro-computed tomography and histomorphometric analysis indicated that the ß-TCP test managed to regenerate more new bone than the untreated ß-TCP and control defects at 8 weeks (p < 0.05). Argon GDP treatment is a viable method for removing macro and micro particles of < 7 µm in size from ß-TCP bigger particles surfaces and therefore improving its biocompatibility with slight surface roughness modification, enhancing hMSCs proliferation, osteoblastic differentiation, and stimulating more new bone formation.

Simple aminophenol-based electrochemical probes for non-enzymatic, dual amperometric detection of NADH and hydrogen peroxide.

Non enzymatic detection of NADH and H2O2 is of practical significance for both environmental and biological prospective. However, there is no simple, straight forward electrochemical sensor available for sensing of them in real samples. Addressing this challenge, we report a simple stimuli responsive aminophenol, pre-anodized screen printed carbon electrode (SPCE*/AP) based electrochemical probes for dual detection of NADH and H2O2. Aminophenol prepared and adsorbed on the electrode from aminophenylboronic acid via boronic acid deprotection with H2O2. The SPCE*/AP fabricated with this process was characterized by cyclic voltammetry (CV), scanning electron microscope (SEM), Raman spectroscopy, UV-visible spectroscopy, and X-ray photoelectron spectroscopy (XPS). Amperometric detection results showed that SPCE*/AP electrodes exhibited linearity from 50 µM to 500 µM and from 200 µM to 2 mM with a detection limit (S/N = 3) of 4.2 µM and 28.9 µM for NADH and H2O2, respectively. Excellent reproducibility and selectivity for NADH and H2O2 were observed for this electrochemical platform. In addition, the matrix effect was investigated further using the same technique to analyze NADH and H2O2 in human urine samples, human serum samples, cell culture medium (containing 10% fetal bovine serum, FBS), and environmental water samples (tap water and rain water). Also, the present sensor demonstrated promising outcomes with living cells (normal cells and cancer cells).

Zingerone Nanotetramer Strengthened the Polypharmacological Efficacy of Zingerone on Human Hepatoma Cell Lines.

We base this study on the concept of drug repositioning to reconstitute the natural product of zingerone as zingerone nanoparticles (zingerone NPs) through a one-pot synthesized process. The as-fabricated zingerone NPs were characterized; they possessed a particle size of 1.42 ± 0.67 nm and a reconstituted structure of zingerone nanotetramer. We further validate the effects of zingerone NPs on the antitumor activity and investigate the relative underlying mechanisms on the human hepatoma SK-Hep-1 and Huh7 cell lines. Our results demonstrated that zingerone NPs significantly inhibit Akt activity and NFκB expression as well as activate the caspases cascade signaling pathway which are involved in the antiproliferation, antitumorigenicity, disturbing cell cycle progression, and induction of DNA damage as well as cell apoptosis. These findings were promising to provide a "Nano-chemoprevention" strategy in future cancer therapeutics and medical and clinical applications.

Anti-cancer effects of 3,5-dimethylaminophenol in A549 lung cancer cells.

Exposure to 3,5-dimethylaminophenol (3,5-DMAP), the metabolite of the 3-5-dimethylaniline, was shown to cause high levels of oxidative stress in different cells. The aim of the present work was to observe whether this metabolite can lead to cytotoxicity, oxidative stress, DNA damage and cell cycle changes in non-small cell lung cancer A549 cells. 3,5-DMAP caused a dose-dependent increase in cytotoxicity, generation of superoxide (O2-.), inductions in the enzyme activities orchestrating cellular antioxidant balance, increases in lipid peroxidation as well as DNA damage. However, 3,5-DMAP showed significantly lower cytotoxicity towards human lung fibroblast (HLF) cells. 3,5-DMAP also led to molecular events, like inducing apoptotic markers (ie. p53, Bad, Bax and cytochrome c); decreasing anti-apoptotic proteins (Bcl-2) and alterations in cell cycle. Our findings indicate that the cytotoxicity caused by this particular alkylaniline metabolite led to initiation of caspase 3-mediated apoptosis. Furthermore, 3,5-DMAP attenuated carcinogenic properties like migration capacity of A549 cells and eventually inhibited growth of A549 cells in an in vivo mouse model. Tumor sections showed that 3,5-DMAP down-regulated c-Myc expression but up-regulated p53 and cytochrome c, all of which might result in tumor growth arrest. Co-treatment with N-acetylcysteine provided reductions in cytotoxicity and positively modulated genetic events induced by 3,5-DMAP in A549 cells. In conclusion, our findings demonstrate 3,5-DMAP may be a potential anti-cancer drug in cancer, due to its self redox cycling properties.

Functional engineered mesenchymal stem cells with fibronectin-gold composite coated catheters for vascular tissue regeneration.

Vascularization of engineered tissues remains one of the key problems. Here, we described a novel approach to promote vascularization of engineered tissues using fibronectin (FN) incorporated gold nanoparticles (AuNP) coated onto catheters with mesenchymal stem cells (MSCs) for tissue engineering. We found that the FN-AuNP composite with 43.5 ppm of AuNP exhibited better biomechanical properties and thermal stability than pure FN. FN-AuNP composites promoted MSC proliferation and increased the biocompatibility. Mechanistically, vascular endothelial growth factor (VEGF) promoted MSC migration on FN-AuNP through the endothelial oxide synthase (eNOS)/metalloproteinase (MMP) signaling pathway. Vascular femoral artery tissues isolated from the implanted FN-AuNP-coated catheters with MSCs expressed substantial CD31 and alpha-smooth muscle actin (α-SMA), displayed higher antithrombotic activity, as well as better endothelialization ability than those coated with all other materials. These data suggested that the implantation of FN-AuNP-coated catheter with MSCs could be a novel strategy for vascular biomaterials applications.

Acute exposure to DEHP metabolite, MEHP cause genotoxicity, mutagenesis and carcinogenicity in mammalian Chinese hamster ovary cells.

Di-(2-ethylhexyl) phthalate (DEHP), the common plasticizer used in the production of polyvinyl chloride, can be converted to the more potent metabolite mono-ethylhexyl phthalate (MEHP). Epidemiological studies have shown an association with elevated induction of rat hepatic cancer and reproductive toxicity in response to MEHP exposure. However, the mechanism of genotoxicity and carcinogenicity induced by MEHP treatment remains unclear. As a means to elucidate the mechanisms of action, lethality and mutagenicity in the adenine phosphoribosyltransferase (aprt+/-) gene induced in several CHO cell types by MEHP were assessed. Dose-response relationships were determined in the parental AA8 cell line, its nucleotide repair-deficient UV5 and base repair-deficient EM9 subclones, and also in AS52 cells harboring the bacterial guanine-hypoxanthine phosphoribosyltransferase (gpt) gene and its derived AS52-XPD-knockdown and AS52-PARP-1-knockdown cells. Treatment of AS52 with MEHP led to intracellular production of reactive oxygen species (ROS) and DNA strand breaks in a dose-dependent manner. Separately, mutations in the gpt gene of AS52 cells were characterized and found to be dominated by G:C to A:T and A:T to G:C transitions. Independent AS52-mutant cell (ASMC) clones were collected for the sequential in vivo xenograft tumorigenic studies, 4 of total 20 clones had aggressive tumor growth. Moreover, microarray analysis indicated miR-let-7a and miR-125b downregulated in ASMC, which might raise oncogenic MYC and RAS level and activate ErbB pathway. Comparative evaluation of the results indicates that the principal mechanism of this mutagenic action is probably to be through generation of ROS, causing base excision damage resulting in carcinogenicity.

A Novel PD-L1-targeting Antagonistic DNA Aptamer With Antitumor Effects.

The PD-1/PD-L1 axis is a major pathway involved in tumor immune evasion. Here, we report the novel PD-L1 antagonizing DNA aptamer (aptPD-L1) and demonstrate an integrated pipeline that expedites therapeutic aptamer development. Aptamer can exert antibody-mimic functions and is advantageous over antibody for its chemically synthetic nature, low immunogenicity, and efficient tissue penetration. Our results showed that aptPD-L1 blocked the binding between human PD-1 and PD-L1. Experiments using murine models showed that aptPD-L1 promoted in vitro lymphocyte proliferation and suppressed in vivo tumor growth without the induction of observable liver or renal toxicity. Analyses on the aptPD-L1-treated tumors further revealed elevated levels of infiltrating CD4+ and CD8+ T cells, intratumoral IL-2, TNF-α, interferon (IFN)-γ and the C-X-C motif chemokines, CXCL9 and CXCL10. The CD8+ T cells in the aptPD-L1-treated tumors had higher CXCR3 expression level compared to the random-sequence oligonucleotides-treated ones. Besides, the length and density of CD31+ intratumoral microvessels were significantly decreased in the aptPD-L1 treatment group. Collectively, our data suggested that aptPD-L1 helps T cell function restoration and modifies tumor microenvironment. These chemokines might orchestrate together to attract more T cells into the tumor tissues to form the positive amplification loop against tumor growth, indicating the translational potential of aptPD-L1 in cancer immunotherapy.

Prominent Vascularization Capacity of Mesenchymal Stem Cells in Collagen-Gold Nanocomposites.

The ideal characteristics of surface modification on the vascular graft for clinical application would be with excellent hemocompatibility, endothelialization capacity, and antirestenosis ability. Here, Fourier transform infrared spectroscopy (FTIR), surface enhanced Raman spectroscopy (SERS), atomic force microscopy (AFM), contact angle (θ) measurement, and thermogravimetric analysis (TGA) were used to evaluate the chemical and mechanical properties of collagen-gold nanocomposites (collagen+Au) with 17.4, 43.5, and 174 ppm of Au and suggested that the collagen+Au with 43.5 ppm of Au had better biomechanical properties and thermal stability than pure collagen. Besides, stromal-derived factor-1α (SDF-1α) at 50 ng/mL promoted the migration of mesenchymal stem cells (MSCs) on collagen+Au material through the α5ß3 integrin/endothelial oxide synthase (eNOS)/metalloproteinase (MMP) signaling pathway which can be abolished by the knockdown of vascular endothelial growth factor (VEGF). The potentiality of collagen+Au with MSCs for vascular regeneration was evaluated by our in vivo rat model system. Artery tissues isolated from an implanted collagen+Au-coated catheter with MSCs expressed substantial CD-31 and α-SMA, displayed higher antifibrotic ability, antithrombotic activity, as well as anti-inflammatory response than all other materials. Our results indicated that the implantation of collagen+Au-coated catheters with MSCs could be a promising strategy for vascular regeneration.

Noncoding RNAs in Tumor Epithelial-to-Mesenchymal Transition.

Epithelial-derived tumor cells acquire the capacity for epithelial-to-mesenchymal transition (EMT), which enables them to invade adjacent tissues and/or metastasize to distant organs. Cancer metastasis is the main cause of cancer-related death. Molecular mechanisms involved in the switch from an epithelial phenotype to mesenchymal status are complicated and are controlled by a variety of signaling pathways. Recently, a set of noncoding RNAs (ncRNAs), including miRNAs and long noncoding RNAs (lncRNAs), were found to modulate gene expressions at either transcriptional or posttranscriptional levels. These ncRNAs are involved in EMT through their interplay with EMT-related transcription factors (EMT-TFs) and EMT-associated signaling. Reciprocal regulatory interactions between lncRNAs and miRNAs further increase the complexity of the regulation of gene expression and protein translation. In this review, we discuss recent findings regarding EMT-regulating ncRNAs and their associated signaling pathways involved in cancer progression.