Chemiresistive gas sensor based on Mo0.5W0.5S2 alloy nanoparticles with good selectivity and ppb-level limit of detection to ammonia.

Transition metal dichalcogenides (TMDs) are promising materials for chemiresistive gas sensor, while TMD alloys (two chalcogenide or/and metal elements) with tunable electronic structures have drawn little attention in gas sensing. Herein, Mo0.5W0.5S2 alloy nanoparticles (NPs) were prepared by a facile sonication exfoliation method and then tested for ammonia sensing. The crystal structure, geometric morphology, and elemental composition of Mo0.5W0.5S2 NPs were investigated. The gas sensing measurements demonstrated Mo0.5W0.5S2 NPs with good response to ammonia at 80 °C with a limit of detection down to 500 part per billion (ppb). The sensor also displayed good stability as well as superb selectivity to ammonia in the presence of interferences, such as methanol, acetone, benzene, and cyclohexane. The theoretical calculations revealed Mo and W atoms at edges (such as Mo0.5W0.5S2 (010)) of sheet-like NPs as the active sites for ammonia adsorption. Electrons donated by the adsorbed ammonia were combined with holes in p-type Mo0.5W0.5S2 NPs, and the concentration of the main charge carrier was reduced, resulting in resistance enhancement.

The CBL-LSD1-CXCL8 axis regulates methionine metabolism in glioma.

Gliomas are the most frequent type of brain tumors, with a high mortality rate and a lack of efficient targeted therapy. Methionine is an essential amino acid, and restriction of methionine in the diet has been found to prevent metabolic diseases and aging, inhibit cancer growth and improve cancer treatment. However, mechanisms of action by which methionine metabolism affects gliomas remain largely unclear. The present study found that methionine starvation of glioma cells significantly increased the expression of CXCL8. Mechanistically, E3 ubiquitin ligase was found to mediate the ubiquitinated degradation of the histone demethylase LSD1 via CBL, reducing LSD1 protein stability and, enhancing H3K4me1 modification of the CXCL8 gene. CXCL8 was found to be involved in regulating the reprogramming of glycerophospholipid metabolism, enabling it to respond to a methionine-deprived environment. CXCL8 expression was significantly higher in glioma than in normal brain tissue samples, with elevated CXCL8 being associated with poor prognosis. In summary, CBL-mediated degradation of LSD1 acts as an anti-braking system and serves as a quick adaptive mechanism for re-remodeling epigenetic modifications. This, in turn, promotes cell proliferation, even in a methionine-restricted environment. Taken together, these findings indicate that the CBL/LSD1/CXCL8 axis is a novel mechanistic connection linking between methionine metabolism, histone methylation and glycerophospholipid reprogramming in the tumor microenvironment.

A Facile Approach for Elemental-Doped Carbon Quantum Dots and Their Application for Efficient Photodetectors.

The present work demonstrates a facile hydrothermal approach to synthesize lanthanide-doped carbon quantum dots (CQDs) with europium and/or gadolinium elements. Taking the advantage of broadband adsorption in the ultraviolet-visible region, the doped QDs are directly used as building blocks for photo-electrochemical (PEC)-type photodetectors (PDs) and their performance is systematically investigated under various conditions. The europium (Eu) and gadolinium (Gd) co-doped (C:EuGd) QDs exhibit better photo-response than the single-elemental doped ones and also show outstanding long-term stability. According to the apparent response to light from 350 to 400 nm, the C:EuGd QDs are demonstrated to hold great potential for narrow-band PDs. This work highlights the practical applications of lanthanide-doped CQDs for PDs, and the results are beneficial for the development of elemental-doped CQDs in general.

Advanced Devices for Tumor Diagnosis and Therapy.

At present, tumor diagnosis is performed using common procedures, which are slow, costly, and still presenting difficulties in diagnosing tumors at their early stage. Tumor therapeutic methods also mainly rely on large-scale equipment or non-intelligent treatment approaches. Thus, an early and accurate tumor diagnosis and personalized treatment may represent the best treatment option for a successful result, and the efforts in finding them are still in progress and mainly focusing on non-destructive, integrated, and multiple technologies. These objectives can be achieved with the development of advanced devices and smart technology that represent the topic of the current investigations. Therefore, this review summarizes the progress in tumor diagnosis and therapy and briefly explains the advantages and disadvantages of the described microdevices, finally proposing advanced micro smart devices as the future development trend for tumor diagnosis and therapy.

Bispecific affibody molecule targeting HPV16 and HPV18E7 oncoproteins for enhanced molecular imaging of cervical cancer.

High-risk human papillomavirus (HPV16 and HPV18) are now widely recognized as responsible for cervical cancer, which remains to be the most common gynecologic malignancy in women worldwide. It is well known that viral oncoproteins E6/E7 play key roles in HPV-associated cervical carcinogenesis. Thus, in vivo detection of the two oncoproteins may provide important diagnostic information influencing patient management. More recently, affibody molecules have been demonstrated to be a promising candidate for development as molecular imaging probes. Based on the two monomeric affibody molecules (ZHPV16E7 and ZHPV18E7) generated in our laboratory, here, we used a peptide linker (Gly4Ser)3 to link ZHPV16E7 and ZHPV18E7 to develop a novel heterodimeric affibody ZHPV16E7-(Gly4Ser)3-ZHPV18E7. Both biosensor and immunofluorescence assays have proved that the heterodimeric affibody molecule targeted simultaneously HPV16 and HPV18E7 proteins by binding to the viral oncoproteins. In vivo tumor-imaging experiments using the Dylight755-labeled heterodimeric affibody revealed that strongly high-contrast tumor retention of the heterodimers occurred in both HPV16- and HPV18-derived tumors of nude mice 0.5 h post-injection. The accumulation of Dylight755-labeled heterodimers in tumors was achieved over 48 h. Therefore, we believe that this novel heterodimeric affibody molecule has great potential utility in molecular imaging in vivo and diagnosis of HPV-associated cervical cancers.

Lanthanide doped carbon dots as a fluorescence chromaticity-based pH probe.

A colorimetric and fluorescent pH probe was designed by doping carbon dots (C-dots) with Eu(III), Tb(III) and 2,6-pyridinedicarboxylic acid (DPA). The resulting nanoparticles were applied as fluorescent indicators for pH values (best detected at excitation/emission wavelengths of 272/545, 614 nm). The pH induced optical effects are due to pH induced variations in energy transfer. The fluorescence of the probe shows a continuous color variation, and a linear change with pH values in the range from 3.0 to 10.0 can be established by using a Commission Internationale de L'Eclairage (CIE) chromaticity diagram. This new kind of pH nanoprobe is more accurate than previously reported pH indicator probes because the pH value can be calculated by using chromaticity coordinates that only depend on the chromaticity. The pH nanoprobe was applied to visualize pH values in human breast adenocarcinoma cells (MCF-7). Graphical abstract Carbon dots modified with Eu(III) and Tb(III) complexes of 2,6-pyridinedicarboxylic acid (DPA) were prepared. The doped carbon dots were used as a pH-sensitive nanosensor. The fluorescence chromaticity of the nanoparticles changes with the variation of pH value.

Clinical management of extra­adrenal myelolipoma in the central nervous system: A case report.

Extra-adrenal myelolipoma (EAM) is a rare benign tumor composed of mature adipose and hematopoietic tissues. Its etiology remains to be elucidated and there are few case reports describing the clinical features and treatment of EAMs in the central nervous system. The present study presented our experience and practice in the clinical management of a case of EAM in the right frontal region. A 56-year-old woman was found to have a space-occupying right frontal lesion on computed tomography (CT) of the head. Unenhanced magnetic resonance imaging (MRI) showed a lesion of ~1.5x1.2 cm. Enhanced whole abdominal CT showed a right presacral mass, 2.0 cm in diameter, with clear margins. The postoperative histopathological findings showed mainly mature adipose tissue mixed with extramedullary hematopoietic components. This confirmed the diagnosis of a (bone) marrow lipoma. Myelolipoma of the central nervous system is extremely rare. to the best of the authors' knowledge, only two cases of intracranial myelolipoma have been reported, and the present study introduced the first case in a Chinese patient reported in English. However, when CT shows high density and MRI shows mixed density in the tumor area even without enhancement, the possibility of myelolipoma should be considered in the differential diagnosis.

PLU1 Promotes the Proliferation and Migration of Glioma Cells and Regulates Metabolism.

OBJECTIVES: PLU1 is upregulated in many cancers, including breast, mammary, colorectal, and hepatocellular carcinoma. However, little is known about the potential metabolic mechanisms of PLU1 in glioma progression. Therefore, we investigated the relationship between PLU1 and glioma development. METHODS: We analyzed the relationship between PLU1 expression and World Health Organization (WHO) grade using clinical databases and verified the role of PLU1 in glioma development using transcriptome sequencing, Western blotting, Cell Counting Kit 8, colony formation, and wound healing assays. The relationship between PLU1 and glioma glucose metabolism was also initially explored by changing the concentration of glucose in the culture medium and was validated by metabolomics and energy metabolism. RESULT: PLU1 expression was closely related to WHO grade and was significantly elevated in tumor tissues compared to nontumor tissues. Knockdown or inhibition of PLU1 inhibits proliferation and migration of glioma cells. In addition, we found that PLU1 expression was closely associated with glioma metabolism by transcriptomic, metabolomic, and energy-related molecular analyses and correlated with glucose metabolism. We also found that glucose concentration affects PLU1 expression, and that PLU1 expression affects intracellular glucose levels. CONCLUSION: PLU1 is a novel regulator of metabolic reprograming and a novel strategy for the treatment of glioma.

Application of 3D printing technology in tumor diagnosis and treatment.

3D printing technology is an increasing approach consisting of material manufacturing through the selective incremental delamination of materials to form a 3D structure to produce products. This technology has different advantages, including low cost, short time, diversification, and high precision. Widely adopted additive manufacturing technologies enable the creation of diagnostic tools and expand treatment options. Coupled with its rapid deployment, 3D printing is endowed with high customizability that enables users to build prototypes in shorts amounts of time which translates into faster adoption in the medical field. This review mainly summarizes the application of 3D printing technology in the diagnosis and treatment of cancer, including the challenges and the prospects combined with other technologies applied to the medical field.

STUB1-SMYD2 Axis Regulates Drug Resistance in Glioma cells.

SET and MYND domain-containing protein 2 (SMYD2) is an important epigenetic regulator that methylates histone and non-histone proteins. The study aimed to investigate the oncogenic role of SMYD2 in gliomas and explore its degradation mechanism induced by cisplatin. Tumor tissue microarray of 441 patients with glioma was collected for SMYD2 immunohistochemical staining. Kaplan-Meier survival curves were constructed using the overall survival values. mRNA-sequencing analysis was performed for understanding the downstream mechanisms mediated by SMYD2. The half-inhibitory concentrations (IC50) of temozolomide and cisplatin in AZ505-treated and control cells were calculated. The potential E3 ubiquitin ligase of SMYD2 was predicted in UbiBrowser and confirmed by a knockdown test. The effect of SMYD2 and its E3 ligase on apoptosis and migration of glioma cells was determined via cell-function assays. High SMYD2 expression correlated with a high WHO stage (P = 0.004) and a low survival probability (P = 0.012). The inhibition of SMYD2 suppressed the process of epithelial to mesenchymal transition (EMT) by downregulating the expression of Collagen 1A1 (COL1A1). AZ505 treatment significantly increased the drug sensitivity of glioma cells. SMYD2 expression was markedly reduced by cisplatin treatment via STIP1 Homology And U-Box Containing Protein 1 (STUB1)-mediated degradation. The knockdown of STUB1 could partly reverse the cell function impairment induced by cisplatin. Our findings suggested that SMYD2 could be a potential drug target for the treatment of gliomas, and STUB1-mediated degradation of SMYD2 plays an important role in reversing chemotherapy resistance in patients with gliomas.

Inhibition of MAT2A-Related Methionine Metabolism Enhances The Efficacy of Cisplatin on Cisplatin-Resistant Cells in Lung Cancer.

Objective: Tumor drug resistance is a vital obstacle to chemotherapy in lung cancer. Methionine adenosyltransferase 2A has been considered as a potential target for lung cancer treatment because targeting it can disrupt the tumorigenicity of lung tumor-initiating cells. In this study, we primarily observed the role of methionine metabolism in cisplatin-resistant lung cancer cells and the functional mechanism of MAT2A related to cisplatin resistance. Materials and Methods: In this experimental study, we assessed the half maximal inhibitory concentration (IC50) of cisplatin in different cell lines and cell viability via Cell Counting Kit-8. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of relative proteins and genes. Crystal violet staining was used to investigate cell proliferation. Additionally, we explored the transcriptional changes in lung cancer cells via RNA-seq. Results: We found H460/DDP and PC-9 cells were more resistant to cisplatin than H460, and MAT2A was overexpressed in cisplatin-resistant cells. Interestingly, methionine deficiency enhanced the inhibitory effect of cisplatin on cell activity and the pro-apoptotic effect. Targeting MAT2A not only restrained cell viability and proliferation, but also contributed to sensitivity of H460/DDP to cisplatin. Furthermore, 4283 up-regulated and 5841 down-regulated genes were detected in H460/DDP compared with H460, and 71 signal pathways were significantly enriched. After treating H460/DDP cells with PF9366, 326 genes were up-regulated, 1093 genes were down-regulated, and 13 signaling pathways were significantly enriched. In TNF signaling pathway, CAS7 and CAS8 were decreased in H460/DDP cells, which increased by PF9366 treatment. Finally, the global histone methylation (H3K4me3, H3K9me2, H3K27me3, H3K36me3) was reduced under methionine deficiency conditions, while H3K9me2 and H3K36me3 were decreased specially via PF9366. Conclusion: Methionine deficiency or MAT2A inhibition may modulate genes expression associated with apoptosis, DNA repair and TNF signaling pathways by regulating histone methylation, thus promoting the sensitivity of lung cancer cells to cisplatin.

The Role of Tumour Metabolism in Cisplatin Resistance.

Cisplatin is a chemotherapy drug commonly used in cancer treatment. Tumour cells are more sensitive to cisplatin than normal cells. Cisplatin exerts an antitumour effect by interfering with DNA replication and transcription processes. However, the drug-resistance properties of tumour cells often cause loss of cisplatin efficacy and failure of chemotherapy, leading to tumour progression. Owing to the large amounts of energy and compounds required by tumour cells, metabolic reprogramming plays an important part in the occurrence and development of tumours. The interplay between DNA damage repair and metabolism also has an effect on cisplatin resistance; the molecular changes to glucose metabolism, amino acid metabolism, lipid metabolism, and other metabolic pathways affect the cisplatin resistance of tumour cells. Here, we review the mechanism of action of cisplatin, the mechanism of resistance to cisplatin, the role of metabolic remodelling in tumorigenesis and development, and the effects of common metabolic pathways on cisplatin resistance.

Adenosinergic Pathway: A Hope in the Immunotherapy of Glioblastoma.

Brain tumors comprise different types of malignancies, most of which are originated from glial cells. Glioblastoma multiforme (GBM) is the most aggressive type of brain tumor with a poor response to conventional therapies and dismal survival rates (15 months) despite multimodal therapies. The development of immunotherapeutic strategies seems to be necessary to enhance the overall survival of GBM patients. So far, the immunotherapies applied in GBM had promising results in the primary phases of clinical trials but failed to continue their beneficial effects in later phases. GBM-microenvironment (GME) is a heterogenic and rigorously immunosuppressive milieu wrapping by an impenetrable blood-brain barrier. Hence, in-depth knowledge about the dominant immunosuppressive mechanisms in the GME could foster GBM immunotherapy. Recently, the adenosinergic pathway (AP) is found to be a major player in the suppression of antitumor immune responses in the GME. Tumor cells evolve to metabolize pro-inflammatory ATP to anti-inflammatory adenosine. Adenosine can suppress immune responses through the signaling of adenosine receptors on immune cells. The preclinical results targeting AP in GBM showed promising results in reinvigorating antitumor responses, overriding chemoresistance, and increasing survival. We reviewed the current GBM immunotherapies and elaborated on the role of AP in the immunopathogenesis, treatment, and even prognosis of GBM. We suggest that future clinical studies should consider this pathway in their combination therapies along with other immunotherapeutic approaches.

Recent advances on TMDCs for medical diagnosis.

Transition metal dichalcogenides (TMDCs), such as MoS2 and WS2, have attracted much attention in biosensing and bioimaging due to its excellent stability, biocompatibility, high specific surface area, and wide varieties. In this review, we overviewed the application of TMDCs in biosensing and bioimaging. Firstly, the synthesis methods and surface functionalization methods of TMDCs were summarized. Secondly, according to the working mechanism, we classified and gave a detailed account of the latest research progress of TMDC-based biosensing for the detection of the enzyme, DNA, and other biological molecules. Then, we outlined the recent progress of applying TMDCs in bio-imaging, including fluorescence, X-ray computed tomographic, magnetic response imaging, photographic and multimodal imaging, respectively. Finally, we discussed the future challenges and development direction of the application of TMDCs in medical diagnosis. Also, we put forward our view on the opportunity of TMDCs in the big data of modern medical diagnosis.

SYVN1-MTR4-MAT2A Signaling Axis Regulates Methionine Metabolism in Glioma Cells.

Methionine is one of the essential amino acids. How tumor cells adapt and adjust their signal transduction networks to avoid apoptosis in a methionine-restricted environment is worthy of further exploration. In this study, we investigated the molecular mechanism of glioma response to methionine restriction, providing a theoretical basis for new treatment strategies for glioma. METHODS: We constructed methionine-restriction-tolerant cells in order to study the response of glioma to a methionine-restricted environment. The transcriptome analysis of the tolerant cells showed significant changes in MAT2A. Western blotting, immunohistochemistry, quantitative real-time PCR, colony formation assays, and other experiments were used to verify the role of MAT2A in glioma genesis. In addition, the regulatory mechanism of MAT2A mRNA nuclear export was investigated by transfection, plasma nucleation separation, and co-immunoprecipitation. RESULTS: Under methionine restriction, glioma cells showed high expression of MAT2A, and an inhibitor of MAT2A reduced the proliferation of tumor cells. The expression of MAT2A was positively correlated with World Health Organization-grade glioma. High expression of MAT2A was related to increased transfer of its mRNA out of the nucleus. The expression of nuclear export regulatory molecule MTR4 could affect the export of MAT2A mRNA. In a methionine-restricted environment, ubiquitination of MTR4 was enhanced, and thus its protein level was reduced. The E3 ubiquitin ligase was verified to be SYVN1. CONCLUSION: In summary, methionine restriction leads to increased ubiquitination of MTR4, which promotes the transfer of MAT2A mRNA out of the nucleus and MAT2A protein expression. MAT2A promotes histone methylation, prompting cells to proliferate in a methionine-restricted environment.

Serine Metabolism Regulates YAP Activity Through USP7 in Colon Cancer.

Metabolic reprogramming is a vital factor in the development of many types of cancer, including colon cancer. Serine metabolic reprogramming is a major feature of tumor metabolism. Yes-associated protein (YAP) participates in organ size control and tumorigenesis. However, the relationship between YAP and serine metabolism in colon cancer is unclear. In this study, RNA sequencing and metabolomics analyses indicated significant enrichment of the glycine, serine, and threonine metabolism pathways in serine starvation-resistant cells. Short-term serine deficiency inhibited YAP activation, whereas a prolonged response dephosphorylated YAP and promoted its activity. Mechanistically, USP7 increases YAP stability under increased serine conditions by regulating deubiquitination. Verteporfin (VP) effectively inhibited the proliferation of colon cancer cells and organoids and could even modulate serine metabolism by inhibiting USP7 expression. Clinically, YAP was significantly activated in colon tumor tissues and positively correlated with the expression of phosphoglycerate dehydrogenase (PHGDH) and USP7. Generally, our study uncovered the mechanism by which serine metabolism regulates YAP via USP7 and identified the crucial role of YAP in the regulation of cell proliferation and tumor growth; thus, VP may be a new treatment for colon cancer.

High ACR level is a strong risk factor for renal tubular impairment in patients with type 2 diabetes: A longitudinal observational study.

BACKGROUND: Several studies have indicated that high albuminuria is associated with renal function decline. However, the relationship between the urinary albumin-to-creatinine ratio (ACR) and risk of developing tubular injury remains unclear. Our aim was to investigate the association of ACR with the risk of developing tubular impairment in patients with type 2 diabetes. METHODS: This longitudinal observational study compared baseline with follow-up data in 183 patients with type 2 diabetes. ACR, urinary alpha-1-microglobulin-to-creatinine ratio (A1MCR) and estimated glomerular filtration rate (eGFR) were used to evaluate albuminuira, tubular injury and glomerular filtration function, respectively. RESULTS: Levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and A1MCR were significantly different at the two-year follow-up compared with baseline levels. Among patients both with baseline ACR above and below 30 mg/g, the percentage with A1MCR > 15 mg/g clearly increased after follow-up (P < 0.05). The risk of A1MCR rising from normal ranges to >15 mg/g over the follow-up increased with increasing baseline ACR values lower baseline eGFR. Among the patients with baseline ACR > 63.10 mg/g, all showed increased A1MCR values at follow-up compared with baseline. In the multivariate regression analysis, the patients with baseline ACR > 63.10 mg/g had a strong risk of A1MCR rising from normal to >15 mg/g (odds ratio (OR) = 11.12, P = 0.001) over the follow-up, while the males had a 2.89-fold risk of A1MCR increasing from normal to >15 mg/g compared with females. CONCLUSION: Baseline ACR level is related to increased risk of developing renal tubular injury; in particular, this association is much stronger in patients with type 2 diabetes and baseline ACR > 63.10 mg/g.

[Expression of HPV16 E6 recombinant protein and preparation of its rabbit polyclonal antibody].

Objective To express E6 protein of human papillomavirus (HPV) type 16 in prokaryotic expression system and prepare its polyclonal antibody. Methods HPV16 E6 gene was obtained from Siha cells by PCR and cloned into pET21a(+) vector to construct the recombinant plasmid pET21a(+)/HPV16 E6 that was confirmed by sequencing. The recombinant plasmid pET21a(+)/HPV16 E6 was transformed into E. coli BL21 (DE3). The HPV16 E6-His tag recombinant protein was expressed after the induction of isopropyl beta-D-1-thiogalactopyranoside (IPTG), purified by Ni-NTA affinity chromatography, and then analyzed by Western blot analysis. The purified HPV16 E6 recombinant protein was used to immunize Japanese white rabbits to prepare polyclonal antibody. The titer of the serum polyclonal antibody was determined by ELISA. The specificity of the polyclonal antibody was analyzed by Western blotting and immunofluorescence. Results The recombinant plasmid pET21a(+)/HPV16 E6 was successfully constructed and confirmed by sequencing. After the recombinant plasmid pET21a(+)/HPV16 E6 was transformed into E. coli BL21 (DE3), the recombinant HPV16 E6 protein was expressed and purified by affinity chromatography. The polyclonal antibody at a titer of 1:40 000 was obtained by immunizing Japanese big-ear white rabbit with the purified recombinant HPV16 E6 protein, and its specificity was confirmed by Western blotting and immunofluorescence assay. Conclusion HPV16 E6 recombinant protein was successfully expressed and the rabbit polyclonal antibody against HPV16 E6 recombinant protein was prepared.

Solution-gated transistors of two-dimensional materials for chemical and biological sensors: status and challenges.

Two-dimensional (2D) materials have been the focus of materials research for many years due to their unique fascinating properties and large specific surface area (SSA). They are very sensitive to the analytes (ions, glucose, DNA, protein, etc.), resulting in their wide-spread development in the field of sensing. New 2D materials, as the basis of applications, are constantly being fabricated and comprehensively studied. In a variety of sensing applications, the solution-gated transistor (SGT) is a promising biochemical sensing platform because it can work at low voltage in different electrolytes, which is ideal for monitoring body fluids in wearable electronics, e-skin, or implantable devices. However, there are still some key challenges, such as device stability and reproducibility, that must be faced in order to pave the way for the development of cost-effective, flexible, and transparent SGTs with 2D materials. In this review, the device preparation, device physics, and the latest application prospects of 2D materials-based SGTs are systematically presented. Besides, a bold perspective is also provided for the future development of these devices.

Generation of novel affibody molecules targeting the EBV LMP2A N-terminal domain with inhibiting effects on the proliferation of nasopharyngeal carcinoma cells.

Nasopharyngeal carcinoma (NPC) induced by latent infection with Epstein-Barr virus (EBV) remains the most common head and neck cancer in Southeast Asia, especially in the southern part of China. It is well known that persistent expression of two EBV latent membrane proteins (LMP1/LMP2A) plays a key role in nasopharyngeal carcinogenesis. Therefore, the therapeutic approach of targeting the LMP1/LMP2A protein and subsequently blocking the LMP1/LMP2A-mediated signalling pathway has been considered for treating patients with NPC. Recently, affibody molecules, a new class of small (~6.5 kDa) affinity proteins, have been confirmed to be powerful generalisable tools for developing imaging or therapeutic agents by targeting specific molecules. In this study, three EBV LMP2A N-terminal domain-binding affibody molecules (ZLMP2A-N85, ZLMP2A-N110 and ZLMP2A-N252) were identified by screening a phage-displayed peptide library, and their high affinity and specificity for the EBV LMP2A N-terminal domain were confirmed by surface plasmon resonance (SPR), indirect immunofluorescence, co-immunoprecipitation and near-infrared small animal fluorescence imaging in vitro and in vivo. Moreover, affibody molecules targeting the EBV LMP2A N-terminal domain significantly reduced the viability of the EBV-positive cell lines C666-1, CNE-2Z and B95-8. Further investigations showed that affibody ZLMP2A-N110 could inhibit the phosphorylation of AKT, GSK-3ß and ß-catenin signalling proteins, leading to suppression of ß-catenin nuclear translocation and subsequent inhibition of c-Myc oncogene expression, which may be responsible for the reduced viability of NPC-derived cell lines. In conclusion, our findings provide a strong evidence that three novel EBV LMP2A N-terminal domain-binding affibody molecules have great potential for utilisation and development as agents for both molecular imaging and targeted therapy of EBV-related NPC.