Research trend of MRI application for lumbar disc degeneration with low back pain: a bibliometric analysis.

Background: Low Back Pain (LBP) is a pervasive and complex musculoskeletal condition affecting over 80% of the global population. Lumbar Disc Degeneration (LDD) significantly contributes to LBP, and MRI is crucial for its diagnosis and understanding. This study aimes to provide a comprehensive bibliometric analysis of MRI research on LDD with LBP, shedding light on research patterns, collaborations, and potential knowledge gaps. Methods: A comprehensive online search was conducted in the Scopus database to retrieve published literature on LDD with LBP. Bibliometric analysis was conducted to assess publication patterns, co-authorship networks, keyword co-occurrence, and co-citation analysis within the MRI applications for LDD research domain. Bibliometric analysis tools such as VOSviewer and the R package "bibliometrix" were utilized for quantitative assessments. Results: A total of 1,619 publications related to MRI and LDD were analyzed. The analysis indicated a consistent annual growth rate of 4.62% in publications related to MRI and lumbar disc degeneration, reflecting a steady increase in research output over the past two decades. The USA, China, and Japan emerged as leading contributors. "SPINE", "European Spine Journal", and "Spine Journal" were the most productive journals in this domain. Key research themes identified included lumbar spine, low back pain, and magnetic resonance imaging. Network visualization shows that low back pain and magnetic resonance imaging were the most widely used keywords. Conclusion: The comprehensive bibliometric analysis of MRI applications for Lumbar Disc Degeneration offers insights into prevailing research patterns, highlights key contributors and journals, and identifies significant research themes. This study provides a foundation for future research efforts and clinical practices in the field, ultimately contributing to the advancement of patient care for individuals suffering from LDD and associated Low Back Pain.

Therapeutic trends of priming mesenchymal stem cells: A bibliometric analysis.

Mesenchymal stem cells (MSCs) have gained substantial attention in regenerative medicine due to their multilineage differentiation potential and immunomodulatory capabilities. MSCs have demonstrated therapeutic promise in numerous preclinical and clinical studies across a variety of diseases, including neurodegenerative disorders, cardiovascular diseases, and autoimmune conditions. Recently, priming MSCs has emerged as a novel strategy to enhance their therapeutic efficacy by preconditioning them for optimal survival and function in challenging in vivo environments. This study presented a comprehensive bibliometric analysis of research activity in the field of priming mesenchymal stem cells (MSCs) from 2003 to 2023. Utilizing a dataset of 585 documents, we explored research trends, leading authors and countries, productive journals, and frequently used keywords. We also explored priming strategies to augment the therapeutic efficacy of MSCs. Our findings show increasing research productivity with a peak in 2019, identified the United States as the leading contributor, and highlighted WANG JA as the most prolific author. The most published journal was Stem Cell Research & Therapy. Keyword analysis revealed core research areas emerging hotspots, while coword and cited sources visualizations elucidated the conceptual framework and key information sources. Further studies are crucial to advance the translation of primed MSCs from bench to bedside, potentially revolutionizing the landscape of regenerative medicine.

In vivo tracking of mesenchymal stem cell dynamics and therapeutics in LPS-induced acute lung injury models.

Mesenchymal stem cells (MSCs) have been widely used to treat various inflammatory and immune-related diseases in preclinical and clinical settings. Intravital microscopy (IVM) is considered the gold standard for investigating pathophysiological conditions in living animals. However, the potential for real-time monitoring of MSCs in the pulmonary microenvironment remains underexplored. In this study, we first constructed a lung window and captured changes in the lung at the cellular level under both inflammatory and noninflammatory conditions with a microscope. We further investigated the dynamics and effects of MSCs under two different conditions. Meanwhile, we assessed the alterations in the adhesive capacity of vascular endothelial cells in vitro to investigate the underlying mechanisms of MSC retention in an inflammatory environment. This study emphasizes the importance of the "lung window" for live imaging of the cellular behavior of MSCs by vein injection. Moreover, our results revealed that the upregulation of vascular cell adhesion molecule 1 (VCAM1) in endothelial cells post-inflammatory injury could enhance MSC retention in the lung, further ameliorating acute lung injury. In summary, intravital microscopy imaging provides a practical method to investigate the therapeutic effects of MSCs in acute lung injury.

Enhancers of mesenchymal stem cell stemness and therapeutic potency.

Mesenchymal stem cells (MSCs) are multipotent stromal cells that can differentiate into a range of cell types, including osteoblasts, chondrocytes, myocytes, and adipocytes. Multiple preclinical investigations and clinical trials employed enhanced MSCs-dependent therapies in treatment of inflammatory and degenerative diseases. They have demonstrated considerable and prospective therapeutic potentials even though the large-scale use remains a problem. Several strategies have been used to improve the therapeutic potency of MSCs in cellular therapy. Treatment of MSCs utilizing pharmaceutical compounds, cytokines, growth factors, hormones, and vitamins have shown potential outcomes in boosting MSCs' stemness. In this study, we reviewed the current advances in enhancing techniques that attempt to promote MSCs' therapeutic effectiveness in cellular therapy and stemness in vivo with potential mechanisms and applications.

Superior protective effects of PGE2 priming mesenchymal stem cells against LPS-induced acute lung injury (ALI) through macrophage immunomodulation.

BACKGROUND: Mesenchymal stem cells (MSCs) have demonstrated remarkable therapeutic promise for acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS). MSC secretomes contain various immunoregulatory mediators that modulate both innate and adaptive immune responses. Priming MSCs has been widely considered to boost their therapeutic efficacy for a variety of diseases. Prostaglandin E2 (PGE2) plays a vital role in physiological processes that mediate the regeneration of injured organs. METHODS: This work utilized PGE2 to prime MSCs and investigated their therapeutic potential in ALI models. MSCs were obtained from human placental tissue. MSCs were transduced with firefly luciferase (Fluc)/eGFP fusion protein for real-time monitoring of MSC migration. Comprehensive genomic analyses explored the therapeutic effects and molecular mechanisms of PGE2-primed MSCs in LPS-induced ALI models. RESULTS: Our results demonstrated that PGE2-MSCs effectively ameliorated lung injury and decreased total cell numbers, neutrophils, macrophages, and protein levels in bronchoalveolar lavage fluid (BALF). Meanwhile, treating ALI mice with PGE2-MSCs dramatically reduced histopathological changes and proinflammatory cytokines while increasing anti-inflammatory cytokines. Furthermore, our findings supported that PGE2 priming improved the therapeutic efficacy of MSCs through M2 macrophage polarization. CONCLUSION: PGE2-MSC therapy significantly reduced the severity of LPS-induced ALI in mice by modulating macrophage polarization and cytokine production. This strategy boosts the therapeutic efficacy of MSCs in cell-based ALI therapy.

Evaluation of Lee-Carter model to breast cancer mortality prediction in China and Pakistan.

Background: Precise breast cancer-related mortality forecasts are required for public health program and healthcare service planning. A number of stochastic model-based approaches for predicting mortality have been developed. The trends shown by mortality data from various diseases and countries are critical to the effectiveness of these models. This study illustrates the unconventional statistical method for estimating and predicting the mortality risk between the early-onset and screen-age/late-onset breast cancer population in China and Pakistan using the Lee-Carter model. Methods: Longitudinal death data for female breast cancer from 1990 to 2019 obtained from the Global Burden of Disease study database were used to compare statistical approach between early-onset (age group, 25-49 years) and screen-age/late-onset (age group, 50-84 years) population. We evaluated the model performance both within (training period, 1990-2010) and outside (test period, 2011-2019) data forecast accuracy using the different error measures and graphical analysis. Finally, using the Lee-Carter model, we predicted the general index for the time period (2011 to 2030) and derived corresponding life expectancy at birth for the female breast cancer population using life tables. Results: Study findings revealed that the Lee-Carter approach to predict breast cancer mortality rate outperformed in the screen-age/late-onset compared with that in the early-onset population in terms of goodness of fit and within and outside forecast accuracy check. Moreover, the trend in forecast error was decreasing gradually in the screen-age/late-onset compared with that in the early-onset breast cancer population in China and Pakistan. Furthermore, we observed that this approach had provided almost comparable results between the early-onset and screen-age/late-onset population in forecast accuracy for more varying mortality behavior over time like in Pakistan. Both the early-onset and screen-age/late-onset populations in Pakistan were expected to have an increase in breast cancer mortality by 2030. whereas, for China, it was expected to decrease in the early-onset population. Conclusion: The Lee-Carter model can be used to estimate breast cancer mortality and so to project future life expectancy at birth, especially in the screen-age/late-onset population. As a result, it is suggested that this approach may be useful and convenient for predicting cancer-related mortality even when epidemiological and demographic disease data sets are limited. According to model predictions for breast cancer mortality, improved health facilities for disease diagnosis, control, and prevention are required to reduce the disease's future burden, particularly in less developed countries.

Prevalence of Intestinal Parasites among Immunocompromised Patients, Children, and Adults in Sana'a, Yemen.

Intestinal parasite infection (IPI) is still a very important public health issue. The severity of the parasitic disease has been reported as a high infection in immunocompromised patients and children. Hence, this study aimed to investigate the prevalence of intestinal parasites among immunocompromised patients and children with various gastrointestinal system complications in Sana'a city, Yemen, with different variables, including genus and age, and explore the risk factors associated with parasitic intestinal infections. The study socioeconomic data and certain behavioral and environmental risk factors and stool samples were collected from immunocompromised adult and children's patients, including children (one to eight years old), pregnant women, diabetes mellitus patients, cancer patients, HIV patients, and older adults. Out of 436 fecal samples, the overall prevalence rate of IPIs among immunocompromised patients and children in Sana'a was 51.8%. In contrast, the rate of infection in children (26.1%) was higher than that in old patients (25.7%) and in females (38.5%) and higher than that in males (13.3%). The protozoa (44.5%) have been shown more than intestinal helminths (7.3%) in samples, and the most common intestinal protozoan was Giardia lamblia and Entamoeba histolytica (13.8% and 12.8%), respectively. The most common intestinal helminthiasis was Hymenolepis nana with 1.8%. Concluding that the rate of infection was high for several reasons, including lack of commitment to hygiene as not handwashing after using the toilet (88.9%), eating uncovered food (56.3%), poor sanitation as lack of water sources (59.5%), reduced health education, and presence of other family members infected by parasites (61.3%). Interventions are required to reduce intestinal parasites, including health education on personal hygiene for patients, increasing awareness, and improving the environment and healthcare system.

Anti-inflammatory Effects of Mesenchymal Stem Cells and their Secretomes in Pneumonia.

Mesenchymal stem cells (MSCs) are multipotent progenitor cells that play crucial roles in the microenvironment of injured tissues. The potential therapeutics of MSCs have attracted extensive attention for several diseases such as acute respiratory distress syndrome (ARDS) and novel coronavirus disease 2019 (COVID-19) pneumonia. MSC-extracellular vesicles have been isolated from MSC-conditioned media (MSC-CM) with similar functional effects as parent MSCs. The therapeutic role of MSCs can be achieved through the balance between the inflammatory and regenerative microenvironments. Clinical settings of MSCs and their extracellular vesicles remain promising for many diseases, such as ARDS and pneumonia. However, their clinical applications remain limited due to the cost of growing and storage facilities of MSCs with a lack of standardized MSC-CM. This review highlights the proposed role of MSCs in pulmonary diseases and discusses the recent advances of MSC application for pneumonia and other lung disorders.

The temporal trend of disease burden attributable to metabolic risk factors in China, 1990-2019: An analysis of the Global Burden of Disease study.

Background and aims: The disease burden attributable to metabolic risk factors is rapidly increasing in China, especially in older people. The objective of this study was to (i) estimate the pattern and trend of six metabolic risk factors and attributable causes in China from 1990 to 2019, (ii) ascertain its association with societal development, and (iii) compare the disease burden among the Group of 20 (G20) countries. Methods: The main outcome measures were disability-adjusted life-years (DALYs) and mortality (deaths) attributable to high fasting plasma glucose (HFPG), high systolic blood pressure (HSBP), high low-density lipoprotein (HLDL) cholesterol, high body-mass index (HBMI), kidney dysfunction (KDF), and low bone mineral density (LBMD). The average annual percent change (AAPC) between 1990 and 2019 was analyzed using Joinpoint regression. Results: For all six metabolic risk factors, the rate of DALYs and death increased with age, accelerating for individuals older than 60 and 70 for DALYs and death, respectively. The AAPC value in rate of DALYs and death were higher in male patients than in female patients across 20 age groups. A double-peak pattern was observed for AAPC in the rate of DALYs and death, peaking at age 20-49 and at age 70-95 plus. The age-standardized rate of DALYs increased for HBMI and LBMD, decreased for HFPG, HSBP, KDF, and remained stable for HLDL from 1990 to 2019. In terms of age-standardized rate of DALYs, there was an increasing trend of neoplasms and neurological disorders attributable to HFPG; diabetes and kidney diseases, neurological disorders, sense organ diseases, musculoskeletal disorders, neoplasms, cardiovascular diseases, digestive diseases to HBMI; unintentional injuries to LBMD; and musculoskeletal disorders to KDF. Among 19 countries of Group 20, in 2019, the age-standardized rate of DALYs and death were ranked fourth to sixth for HFPG, HSBP, and HLDL, but ranked 10th to 15th for LBMD, KDF, and HBMI, despite the number of DALYs and death ranked first to second for six metabolic risk factors. Conclusions: Population aging continuously accelerates the metabolic risk factor driven disease burden in China. Comprehensive and tight control of metabolic risk factors before 20 and 70 may help to mitigate the increasing disease burden and achieve healthy aging, respectively.

The efficacy and safety of Nivolumab combined with Ipilimumab in the immunotherapy of cancer: a meta-analysis.

Background and Objective: Nivolumab and Ipilimumab are immune checkpoint inhibitors. The combination of Nivolumab and Ipilimumab has been reported to have complementary effects in the treatment of metastatic melanoma. The combination therapy of Nivolumab and Ipilimumab (N+I) has shown synergistic effects in cancer immunotherapy but this is still controversial due to the higher incidence of toxicity. Hence, we conducted a meta-analysis to evaluate the efficacy and safety profile of Nivolumab combined with Ipilimumab and compared the different dosing schedules of the N+I combination.Methods: By searching in PubMed, PMC, Cochrane library and major conference abstracts, eligible sixteen studies including N+I therapy and Nivolumab monotherapy were selected to analyze overall response rate (ORR), progression-free survival (PFS), overall survival (OS), and high-grade (3-4) adverse effects (AEs). Results: Compared with monotherapy of Nivolumab, N+I significantly improved ORR (RR=1.40 [95% CI 1.27, 1.54], P<0.00001) and PFS (Hazard Ratio (HR)=0.83 [95% CI 0.77, 0.90], P<0.00001), but not OS (HR=0.93 [95% CI 0.84, 1.03], P=0.16). In a sub-analysis, the combination of Nivolumab 1mg/kg plus Ipilimumab 3mg/kg (N1I3) and Nivolumab 3mg/kg plus Ipilimumab 1mg/kg (N3I1) achieved better ORR and PFS than Nivolumab 3mg/kg (N3) alone. Remarkably, OS was also prolonged with the N1I3 combination compared with the N3I1 combination or N3. Furthermore, a higher incidence of high-grade AEs also occurred with the combination therapy of N1I3.Conclusions: N+I combination therapy showed greater ORR and PFS compared with Nivolumab monotherapy. N1I3 combination provided the benefit of ORR, PFS and OS but was associated with a higher incidence of toxicity.

Recent insights of the role and signalling pathways of interleukin-34 in liver diseases.

Liver disease is a global health problem and is a primary cause of mortality and morbidity worldwide. Specifically, it accounts for approximately two million deaths per year worldwide. The common causes of mortality are the complications of liver cirrhosis, viral hepatitis and hepatocellular carcinoma (HCC). The mechanism of immune response and infiltration of cellular immunity is essential for promoting hepatic inflammatory, especially when the liver is abundant with lymphocytes and phagocytic cells. The injured and immunity cells secret different types of interleukins (cytokines), which can directly or indirectly amplify or inhibit liver inflammation. Many types of cells can produce interleukin-34 (IL-34) that induces the release of multiple inflammatory factors in patients via interaction with various cytokines. This phenomenon leads to the enlargement of the inflammatory response to liver diseases and induces liver fibrosis. This review highlights the proposed roles of IL-34 in liver diseases and discusses the recent findings of IL-34 that support its emerging role in HCC. Specifically, the facilitating effects of these new insights on the rational development of IL-34 for targeted therapies in the future are explored.

Diacerein: Recent insight into pharmacological activities and molecular pathways.

Diacerein is a symptomatic slow-acting drug in osteoarthritis (SYSADOA) and the active metabolite is rhein. It is a non-steroidal anti-inflammatory drug with unique pharmacological properties as anti-oxidant and anti-apoptosis. Diacerein has recently shown to have a potential role by mediating anti-inflammatory as well as anti-oxidant and anti-apoptosis in kidney injury, diabetes mullites, and a beneficial effect on pain relief. It may have a therapeutic role in cancer, ulcerative colitis, testicular injury and cervical hyperkeratosis. Furthermore, diacerein has a valuable addition in combination therapy as a synergetic agent. This review, the first of its kind, highlights the proposed roles of diacerein in osteoarthritis and discusses recent results supporting its emerging roles with a particular focus on how these new insights may facilitate the rational development of diacerein for targeted therapies in the future.

Enhanced therapeutic effects of MSC-derived extracellular vesicles with an injectable collagen matrix for experimental acute kidney injury treatment.

BACKGROUND: Mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) have been shown to have therapeutic potential for ischemic diseases and are considered an alternative to cell therapy. However, the low retention and poor stability of EVs post-transplantation in vivo remain obstacle prior to the clinical application of EVs. METHODS: This study was designed to investigate whether collagen matrix could increase the retention and stability of EVs and further improve the therapeutic effects in murine acute kidney injury (AKI) model. EVs were isolated from human placental MSCs (hP-MSC-EVs) and encapsulated in a collagen matrix. Then, we investigated whether collagen matrix can prolong the retention of EVs in vivo, further enhancing the therapeutic efficiency of EVs in AKI. RESULTS: Our results indicated that collagen matrix could effectively encapsulate EVs, significantly increase the stability of EVs, and promote the sustained release of EVs. Collagen matrix has improved the retention of EVs in the AKI model, which was proved by Gaussia luciferase (Gluc) imaging. The application of collagen matrix remarkably facilitated the proliferation of renal tubular epithelial cells in AKI compared with EVs alone. Moreover, collagen matrix could further augment the therapeutic effects of hP-MSC-EVs as revealed by angiogenesis, fibrosis and apoptosis, and functional analysis. Finally, we found that EVs play a therapeutic role by inhibiting endoplasmic reticulum (ER) stress. CONCLUSIONS: Collagen matrix markedly enhanced the retention of EVs and further augmented the therapeutic effects of EVs for AKI. This strategy for improving the efficacy of EVs therapy provides a new direction for cell-free therapy.

CD24 targeting bi-specific antibody that simultaneously stimulates NKG2D enhances the efficacy of cancer immunotherapy.

PURPOSE: Bi-specific antibody (BsAb) is an emerging novel format of antibody. We aimed to develop the natural killer (NK) cell receptor NK group 2, member D (NKG2D)-mediated, immune surveillance system. In this system, the NKG2D ligand MHC class I-related chain A (MICA) was fused with BsAb, which targeted a cluster of differentiation 24 (CD24), a tumor-initiating cell marker that is over-expressed on hepatocellular carcinoma (HCC). METHODS: The Homo MICA extracellular domains (hMICA) were fused to the end of the heavy chain of cG7 with the flexible pentapeptide (Gly-Gly-Gly-Gly-Ser; G4S), which formed the cG7-MICA that was further identified using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and western blotting (WB). The targeting specificity was characterized using the Surface Plasmon Resonance (SPR) technology and a flow cytometry assay. Furthermore, the design of BsAb cG7-MICA that targeted CD24 and NKG2D was proven to enhance antibody-dependent, cell-mediated cytotoxicity (ADCC) in vitro by the CytoTox 96 Nonradioactive Cytotoxicity assay. Degranulation and a cytokine production assay of NK cells demonstrated that NK cells were activated effectively by cG7-MICA. Further, in HCC-bearing nude mice, the anti-tumor effects of cG7-MICA combined with sorafenib were verified again. RESULTS: We purified cG7-MICA successfully, and it has a high affinity. In vivo, cG7-MICA recruited NK cells to the tumor site and improved the anti-tumor efficacy of sorafenib. cG7-MICA also activated NK cells to release interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α), and it increased the CD107a expression on the surface of the NK cells in vitro. CONCLUSION: NK cells play a major role in the natural, innate immune system, and they have the function of identifying and killing target cells. cG7-MICA remodels the function of MICA molecules to activate NK cells, which provides a possible strategy for HCC-targeting immunotherapy.

Design, synthesis and evaluation of a novel series of inhibitors reversing P-glycoprotein-mediated multidrug resistance.

Multidrug resistance (MDR) is still the main barrier to attaining effective results with chemotherapy. Discovery of new chemo-reversal agents is needed to overcome MDR. Our study focused on a better way to obtain novel drugs with triazole rings that have an MDR reversal ability through click chemistry. Among 20 developed compounds, compound 19 had a minimal cytotoxic effect compared to tariquidar and verapamil (VRP) and showed a higher reversal activity than VRP through increased accumulation in K562/A02 cells. Compound 19 also played an important role in the P-gp efflux function of intracellular Rh123 and doxorubicin (DOX) accumulation in K562/A02 cells. Moreover, compound 19 exhibited a long lifetime of approximately 24 hr. These results indicated that compound 19 is a potential lead compound for the design of new drugs to overcome cancer MDR.

Antioxidant effects and mechanism of silymarin in oxidative stress induced cardiovascular diseases.

Cardiovascular diseases (CVDs) are considered as the major reason for mortality and morbidity worldwide. Substantial evidence suggests that increased oxidative stress plays a significant role in the pathogenesis of CVDs, including atherosclerosis, hypertension, vascular endothelial dysfunction and ischemic heart disease. Cellular oxidative stress results in the release of toxic free radicals by endothelial cells and vascular smooth muscle cells that interact with cell components such as protein, DNA or lipid resulting in cardiovascular pathology. Silymarin has antioxidant activities against CVDs and offers protection against oxidative stress-induced hypertension, atherosclerosis and cardiac toxicity. We present a comprehensive review regarding the oxidative stress and protective effects of silymarin in CVDs management. We also aim to provide mechanistic insight of the mechanisms of silymarin action in oxidative stress-induced CVDs.

NKG2D Immunoligand rG7S-MICA Enhances NK Cell-mediated Immunosurveillance in Colorectal Carcinoma.

Colorectal carcinoma (CRC) is one of the most common malignant cancers worldwide. The poor response of CRC to chemotherapy has whipped up the interest in targeted therapy with monoclonal antibodies for its potential efficiency. However, cetuximab, as one of the first-line targeted drugs in the treatment of CRC, has drug resistance and poor prognosis in clinic. To address this, a novel bispecific protein with CRC targeting and natural killer (NK) cell triggering was used for treatment. NK cell-mediated immunosurveillance is normally activated by the activating receptor natural killer cell receptor NK group 2, member D (NKG2D), which binds its key ligand major histocompatibility complex (MHC) class I-related chain A (MICA) expressed on the tumor cells. To trigger NK cell-mediated cytotoxicity, we fused MICA portion to a single-chain antibody fragment rG7S targeting the tumor-associated antigen CD24. In vitro, flow cytometry, cytotoxicity assay, degranulation, and cytokines release assay revealed that the fusion protein rG7S-MICA could both binds to CD24 and NKG2D which enhances NK cell sensitivity and NKG2D-mediated immunosurveillance against CD24 CRC cells. Furthermore, in a CD24 CRC-bearing nude mice model, rG7S-MICA effectively recruits NK cell to the tumor site and increase the release of cytokines such as interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α), and shows potential antitumor effects. In conclusion, rG7S-MICA provides a novel immunotherapeutic strategy for CRC, which could be further developed against other CD24 malignancies.

Artemin promotes oncogenicity, metastasis and drug resistance in cancer cells.

Artemin (ARTN) is a member of glial cell line-derived neurotrophic factor (GDNF) family of ligands, and its signaling is mediated via a multi-component receptor complex including the glycosylphosphatidylinositol-anchored GDNF family receptors a (GFRa1, GFRa3) and RET receptor tyrosine kinase. The major mechanism of ARTN action is via binding to a non-signaling co-receptor. The major function of ARTN is to drive the molecule to induce migration and axonal projection from sympathetic neurons. It also promotes the survival, proliferation and neurite outgrowth of sympathetic neurons in vitro. ARTN triggers oncogenicity and metastasis by the activation of the AKT signaling pathway. Recent studies have reported that the expression of ARTN in hepatocellular carcinoma is associated with increased tumor size, quick relapse and shorter survival. Furthermore, ARTN promotes drug resistance such as antiestrogens, doxorubicin, fulvestrant, paclitaxel, tamoxifen and trastuzumab. Moreover, ARTN also stimulates the radio-therapeutic resistance. This review highlights the proposed roles of ARTN in cancer cells and discusses recent results supporting its emerging role as an oncogenic, metastatic and drug-resisting agent with a special focus on how these new insights may facilitate rational development of ARTN for targeted therapies in the future.