Ultrastable, Superrobust, and Recyclable Supramolecular Polymer Networks.

Supramolecular polymer networks (SPNs), crosslinked by noncovalent bonds, have emerged as reorganizable and recyclable polymeric materials with unique functionality. However, poor stability is an imperative challenge faced by SPNs, because SPNs are susceptible to heat, water, and/or solvents due to the dynamic and reversible nature of noncovalent bonds. Herein, the design of a noncovalent cooperative network (NCoN) to simultaneously stabilize and reinforce SPNs is reported, resulting in an ultrastable, superrobust, and recyclable SPN. The NCoN is constructed by multiplying the H-bonding sites and tuning the conformation/geometry of the H-bonding segment to optimize the multivalence cooperativity of H-bonds. The rationally designed H-bonding segment with high conformational compliance favors the formation of tightly packed H-bond arrays comprising higher-density and stronger H-bonds. Consequently, the H-bonded crosslinks in the NCoN display a covalent crosslinking effect but retain on-demand dynamics and reversibility. The resultant ultrastable SPN not only displays remarkable resistance to heat up to 120 °C, water soaking, and a broad spectrum of solvents, but also possesses a superhigh true stress at break (1.1 GPa) and an ultrahigh toughness (406 MJ m-3 ). Despite the covalent-network-like stability, the SPN is recyclable through activating its reversibility in a high-polarity solvent heated to a threshold temperature.

Stretchable Ionic Conductors for Soft Electronics.

With the rapid development of soft electronics in the era of Internet of Everything (IoE), electrical conductors with stretchability, the indispensable components of soft electronics, have gained new opportunities and also faced increasing challenges. According to the principles of electrical conductivity, stretchable electrical conductors can be divided into electronic conductors and ionic conductors. Different from the stretchable electronic conductors derived from stretchable polymeric matrices integrated with electronically conductive fillers, stretchable ionic conductors are constructed by embedding mobile ions into the crosslinked polymer networks. Therefore, stretchable ionic conductors have received extensive attention and in-depth research in the past decade, thanks to their intrinsic stretchability and electrical conductivity. This review systematically summarizes the achievements on the different categories of stretchable ionic conductors (e.g., hydrogels, ionogels, and liquid-free ion-conductive elastomers), in terms of their design, fabrication, properties, and applications. The advantages and limitations of the different types of stretchable ionic conductors are discussed. Outlooks are also provided to envision the remaining challenges for the further development and practical applications of stretchable ionic conductors. It is expected to arouse inspirations for the design and fabrication of new and high-performance stretchable ionic conductors and advanced soft electronics for the IoE era.

Thermal Dynamic Self-Healing Supramolecular Dopant Towards Efficient and Stable Flexible Perovskite Solar Cells.

Flexible perovskite solar cells (FPSCs) have attracted great attention due to their advantageous traits such as low cost, portability, light-weight, etc. However, mechanical stability is still the weak point in their practical application. Herein, we prepared efficient FPSCs with remarkable mechanical stability by a dynamic thermal self-healing effect, which can be realized by the usage of a supramolecular adhesive. The supramolecular adhesive, which was obtained by random copolymerization of acrylamide and n-butyl acrylate, is amphiphilic, has a proper glass transition temperature and a high density of hydrogen-bond donors and receptors, providing the possibility of thermal dynamic repair of mechanical damage in FPSCs. The adhesive also greatly improves the leveling property of the precursor solution on the hydrophobic poly[bis(4-phenyl)(2,4,6-trimethylphenyl)]amine (PTAA) surface. PSCs containing this adhesive achieve more than a 20 % power conversion efficiency (PCE) on flexible substrates and a 21.99 % PCE on rigid substrates (certified PCE of 21.27 %), with improved electron mobility and reduced defect concentration.

Effect of almonertinib on the proliferation, invasion, and migration in non-small cell lung cancer cells. / 阿美替尼对非小细胞肺癌细胞增殖、侵袭和迁移的影响.

OBJECTIVES: Lung cancer is one of the most common malignant tumors in the world, and its lethality ranks the first among many malignant tumors. For non-small cell lung cancer (NSCLC) patients, due to the high mortality rate, the overall 5-year survival rate is less than 15%. When NSCLC undergoes local invasion, the 5-year survival rate is only 20%, and it is even lower when distant metastasis occurs up to 4%. Almonertinib is an innovative drug independently researched and developed by China with independent intellectual property rights. As an epidermal growth factor receptor tyrosine kinase inhibitor, almonertinib is mainly used for locally advanced or metastatic NSCLC patients with epidermal growth factor receptor (EGFR) T790M mutation. This study aims to investigate the effects of almonertinib on the proliferation, invasion and migration of NSCLC cells in vitro. METHODS: NSCLC cells H1975 and PC-9 were cultured in vitro. The effects of almonertinib on the proliferation, apoptosis, invasion, and migration of H1975 and PC-9 cells were detected by CCK-8 assay, apoptotic assay and Transwell assay. The expression of invasion and migration related proteins was detected by Western blotting. RESULTS: The CCK-8 experiment showed that almonertinib inhibited the proliferation of H1975 and PC-9 cells in a time- and dose-dependent manner. The IC50 values in PC-9 cells at 24 and 48 h were 5.422 and 1.302 µmol/L, respectively. The IC50 values in H1975 cells at 24 and 48 h were 4.803 and 2.094 µmol/L, respectively. Almonertinib (1, 2, 4, 8 µmol/L)-treated PC-9 and H1975 cells for 24 h resulted in apoptosis rate at (8.82±3.22)%, (9.53±4.24)%, (13.62±3.69)%, (42.10±1.76)% and (9.81±0.90)%, (10.51±1.49)%, (15.34±3.50)%, (28.97±2.57)%, respectively. The transwell experiment showed that almonertinib inhibited the invasion and migration of H1975 and PC-9 cells. Western blotting showed that compared with the control group, the expression levels of MMP-9, MMP-2 and vimentin protein in PC-9 and H1975 cells in 1, 2 and 4 µmol/L almonertinib treatment group were significantly lower, and the expression level of E-cadherin protein was significantly higher (all P<0.05). The experimental results of nude mice showed that compared with the control group and the positive control ositinib (AZD9291) group, the tumor growth was significantly inhibited, the weight of nude mice, the tumor volume and the tumor mass were significantly reduced in the almonertinib treatment group (all P<0.05). CONCLUSIONS: Almonertinib can inhibit the proliferation, invasion, and migration of NSCLCH1975 and PC-9 cells in vitro and vivo, and promote the apoptosis of H1975 and PC-9 cells. The underlying mechanism may be related to the inhibition of tumor cell epithelial mesenchymal transformation and metalloproteinase expression.

Solvent-Free and Skin-Like Supramolecular Ion-Conductive Elastomers with Versatile Processability for Multifunctional Ionic Tattoos and On-Skin Bioelectronics.

The development of stable and biocompatible soft ionic conductors, alternatives to hydrogels and ionogels, will open up new avenues for the construction of stretchable electronics. Here, a brand-new design, encapsulating a naturally occurring ionizable compound by a biocompatible polymer via high-density hydrogen bonds, resulting in a solvent-free supramolecular ion-conductive elastomer (SF-supra-ICE) that eliminates the dehydration problem of hydrogels and possesses excellent biocompatibility, is reported. The SF-supra-ICE with high ionic conductivity (>3.3 × 10-2  S m-1 ) exhibits skin-like softness and strain-stiffening behaviors, excellent elasticity, breathability, and self-adhesiveness. Importantly, the SF-supra-ICE can be obtained by a simple water evaporation step to solidify the aqueous precursor into a solvent-free nature. Therefore, the aqueous precursor can act as inks to be painted and printed into customized ionic tattoos (I-tattoos) for the construction of multifunctional on-skin bioelectronics. The painted I-tattoos exhibit ultraconformal and seamless contact with human skin, enabling long-term and high-fidelity recording of various electrophysiological signals with extraordinary immunity to motion artifacts. Human-machine interactions are achieved by exploiting the painted I-tattoos to transmit the electrophysiological signals of human beings. Stretchable I-tattoo electrode arrays, manufactured by the printing method, are demonstrated for multichannel digital diagnosis of the health condition of human back muscles and spine.

Highly Transparent and Self-Healable Solar Thermal Anti-/Deicing Surfaces: When Ultrathin MXene Multilayers Marry a Solid Slippery Self-Cleaning Coating.

Solar anti-/deicing can solve icing problems by converting sunlight into heat. One of the biggest problems, which has long been plaguing the design of solar anti-/deicing surfaces, is that photothermal materials are always lightproof and appear black, because of the mutual exclusiveness between generating heat and retaining transparency. Herein, a highly transparent and scalable solar anti-/deicing surface is reported, which enables the coated glass to exhibit high transparency (>77% transmittance at 550 nm) and meanwhile causes a >30 °C surface temperature increase relative to the ambient environment under 1.0 sun illumination. Such a transparent anti-/deicing surface can be fabricated onto a large class of substrates (e.g., glass, ceramics, metals, plastics), by applying a solid omniphobic slippery coating onto layer-by-layer-assembled ultrathin MXene multilayers. Hence, the surface possesses a self-cleaning ability to shed waterborne and oil-based liquids thanks to residue-free slipping motion. Passive anti-icing and active deicing capabilities are, respectively, obtained on the solar thermal surface, which effectively prevents water from freezing and simultaneously melts pre-formed ice and thick frost. The self-cleaning effect enables residue-free removal of unfrozen water and interfacially melted ice/frost to boost the anti-/deicing efficiency. Importantly, the surface is capable of self-healing under illumination to repair physical damage and chemical degradation.

Hedyotis diffusa injection induces ferroptosis via the Bax/Bcl2/VDAC2/3 axis in lung adenocarcinoma.

BACKGROUND: Lung cancer has the highest mortality rate among all cancer types. In combination with multiple chemotherapeutic options, traditional Chinese medicine has proven indispensable for the comprehensive treatment of lung cancer. PURPOSE: To investigate the effects of Hedyotis diffusa on lung adenocarcinoma cell lines and a BALB/c nude mouse xenograft model, and determine whether HDI could induce ferroptosis in lung adenocarcinoma cells along with the underlying mechanism. METHODS: The anti-tumor activity of HDI was determined in vitro by cell counting kit-8, clonogenic, and transwell assays. Subsequently, electron microscopy, a lipid reactive oxygen species assay, ferrous ion staining, and a malondialdehyde assay were performed to determine the effect on ferroptosis in lung adenocarcinoma cells. The mechanism was then further investigated using small molecule inhibitors, siRNA, and plasmid overexpression in vitro. Finally, the effects of HDI were assessed in tumor-bearing BALB/c nude mice, and HE staining was performed to observe tissue damage after HDI treatment. RESULTS: In vitro experiments showed that HDI could inhibit the viability of lung adenocarcinoma cells and induce lung adenocarcinoma cells ferroptosis via mechanisms independent of GPX4 and PUFA-PLS pathways but closely associated with VDAC2/3. HDI regulated VDAC2/3 activity by promoting Bax via inhibiting Bcl2, thereby inducing ferroptosis in lung adenocarcinoma cells. Furthermore, in vivo experiments showed that HDI significantly inhibited the growth of subcutaneous tumors in BALB/c nude mice with less organ damage and toxicity, and significantly increased the expression of the ferroptosis-related indicators 4HNE, TFR, and HMOX1 in tumor tissue. CONCLUSION: HDI can significantly reduce the survival of lung adenocarcinoma cells in vitro, inhibit the growth of subcutaneously transplanted tumors in BALB/c nude mice in vivo, and induce ferroptosis in lung adenocarcinoma cells via Bcl2 inhibition to promote Bax regulation of VDAC2/3.

WITHDRAWN: Anti-lung Cancer Mechanism of Hedyotis Diffusa Willd Based on Network Pharmacology and Molecular Docking

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Sodium cantharidate promotes autophagy in breast cancer cells by inhibiting the PI3K-Akt-mTOR signaling pathway.

Sodium cantharidate (SCA) is a derivative of cantharidin obtained by its reaction with alkali. Studies have shown that it inhibits the occurrence and progression of several cancers. However, therapeutic effects of SCA on breast cancer are less well studied. This study aimed to clarify the effect of SCA on breast cancer cells and its mechanism, and to provide a scientific basis for the clinical use of SCA for the treatment of breast cancer. The results of cell counting kit-8, colony formation assay, and 5-ethynyl-2'-deoxyuridine staining showed that SCA inhibited breast cancer cell proliferation. Wound-healing and transwell assays demonstrated that SCA inhibited the migration and invasion of breast cancer cells. Transmission electron microscopy revealed that SCA induced autophagy in breast cancer cells. RNA sequencing technology showed that SCA significantly regulated the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin (PI3K-Akt-mTOR) pathway, which was further verified using western blotting. The inducing effect of SCA on breast cancer autophagy was reversed by the mTOR activator MHY1485. In addition, subcutaneous xenograft experiments confirmed that SCA significantly inhibited tumor growth in vivo. Hematoxylin-eosin, TdT-mediated dUTP nick-end labeling, and immunohistochemical staining indicated that SCA induced tumor cell autophagy and apoptosis in nude mice without causing organ damage. In summary, we found that SCA promoted breast cancer cell apoptosis by inhibiting the PI3K-Akt-mTOR pathway and inducing autophagy.

Healable and Recyclable Elastomers with Record-High Mechanical Robustness, Unprecedented Crack Tolerance, and Superhigh Elastic Restorability.

Spider silk is one of the most robust natural materials, which has extremely high strength in combination with great toughness and good elasticity. Inspired by spider silk but beyond it, a healable and recyclable supramolecular elastomer, possessing superhigh true stress at break (1.21 GPa) and ultrahigh toughness (390.2 MJ m-3 ), which are, respectively, comparable to and ≈2.4 times higher than those of typical spider silk, is developed. The elastomer has the highest tensile strength (ultimate engineering stress, 75.6 MPa) ever recorded for polymeric elastomers, rendering it the strongest and toughest healable elastomer thus far. The hyper-robust elastomer exhibits superb crack tolerance with unprecedentedly high fracture energy (215.2 kJ m-2 ) that even exceeds that of metals and alloys, and superhigh elastic restorability allowing dimensional recovery from elongation over 12 times. These extraordinary mechanical performances mainly originate from the meticulously engineered hydrogen-bonding segments, consisting of multiple acylsemicarbazide and urethane moieties linked with flexible alicyclic hexatomic spacers. Such hydrogen-bonding segments, incorporated between extensible polymer chains, aggregate to form geometrically confined hydrogen-bond arrays resembling those in spider silk. The hydrogen-bond arrays act as firm but reversible crosslinks and sacrificial bonds for enormous energy dissipation, conferring exceptional mechanical robustness, healability, and recyclability on the elastomer.

Experimental Study of Almonertinib Crossing the Blood-Brain Barrier in EGFR-Mutant NSCLC Brain Metastasis and Spinal Cord Metastasis Models.

Roughly one third of non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI)-sensitive mutated (EGFRm) tumors experience disease progression through central nervous system (CNS) metastases during treatment. Although EGFR-TKIs have been reported to be favored in some patients with EGFRm NSCLC CNS metastases, novel EGFR-TKIs with proven efficacy in CNS pathologies are clinically needed.To investigate whether almonertinib, a novel third-generation EGFR-TKI for NSCLC, can cross the blood-brain barrier (BBB) and deliver treatment for EGFR-mutant NSCLC brain metastases and spinal cord metastases, we constructed NSCLC brain metastasis and spinal cord metastasis models in vivo to observe the anti-tumor effects of almonertinib. Using ABCB1-MDCK and BCRP-MDCK monolayer cells as the in vitro study model, the effects of transport time and drug concentration on the apparent permeability coefficient of almonertinib and its active metabolite, HAS-719, were investigated. The results of this study show that almonertinib can significantly inhibit PC9 brain and spinal cord metastases. Pharmacokinetic studies in mice revealed that almonertinib has good BBB penetration ability, whereas the metabolite HAS-719 does not easily penetrate the BBB. Early clinical evidence of almonertinib activity in patients with EGFRm-advanced NSCLC and brain metastases has also been reported. In conclusion, almonertinib easily penetrates the BBB and inhibits advanced NSCLC brain and spinal cord metastases.

Remalleable, Healable, and Highly Sustainable Supramolecular Polymeric Materials Combining Superhigh Strength and Ultrahigh Toughness.

To build a sustainable society, it is of significant importance but highly challenging to develop remalleable, healable, and biodegradable polymeric materials with integrated high strength and high toughness. Here, we report a superstrong and ultratough sustainable supramolecular polymeric material with a toughness of ca. 282.3 J g-1 (395.2 MJ m-3) in combination with a tensile strength as high as ca. 104.2 MPa and a Young's modulus of ca. 3.53 GPa. The toughness is even higher than that of the toughest spider silk (ca. 354 MJ m-3) ever found in the world, while the material also exhibits a superior tensile strength over most engineering plastics. This material is fabricated by topological confinement of the biodegradable linear polymer of poly(vinyl alcohol) (PVA) via the naturally occurring dendritic molecules of tannic acid (TA) based on high-density hydrogen bonds. Simply blending TA and PVA in aqueous solutions at acidic conditions leads to the formation of TA-PVA complexes as precipitates, which can be processed into dry TA-PVA composite products with desired shapes via the compression molding method. Compared to the conventional solution casting method for the fabrication of PVA-based thin films, the as-developed strategy allows large-scale production of bulk TA-PVA composites. The TA-PVA composites consist of interpenetrating three-dimensional supramolecular TA-PVA clusters. Such a structural feature, revealed by computational simulations, is crucial for the integrated superhigh strength and ultrahigh toughness of the material. The biodegradable TA-PVA composites are remalleable for multiple generations of recycling and healable after break, at room temperature, by the assistance of water to activate the reversibility of the hydrogen bonds. The TA-PVA composites show high promise as sustainable substitutes for conventional plastics because of their remalleability, healability, and biodegradability. The integrated superhigh strength and ultrahigh toughness of the TA-PVA composites ensure their high reliability and broad applicability.

Nicotine promotes cervical metastasis of oral cancer by regulating peroxiredoxin 1 and epithelial-mesenchymal transition in mice.

BACKGROUND: Tobacco is a major risk factor for oral squamous cell carcinoma (OSCC). However, the role of nicotine in OSCC is not completely understood. MATERIALS AND METHODS: To analyze the mechanisms of nicotine-induced cervical metastasis, we investigated whether nicotine induced invasion, migration, and epithelial-mesenchymal transition (EMT) via regulating peroxiredoxin 1 (Prx1) in CAL 27 cells. In addition, we established a mouse model to confirm the roles of nicotine in regulating Ets1/Prx1/EMT signaling in OSCC metastasis. RESULTS: We showed that nicotine induced CAL 27 cell invasion, migration, EMT, and Prx1 and Ets1 expression. Prx1 knockdown inhibited cell invasion, migration, and EMT. Ets1 silencing downregulated Prx1 expression and EMT. Prx1 and Ets1 were shown to interact in CAL 27 cells treated with nicotine, and nicotine could significantly upregulate the binding of the transcription factor Ets1 to the Prx1 gene promoter region. Additionally, an in vivo study showed that nicotine induced tumor metastasis and EMT. Prx1 knockdown inhibited cervical metastasis rates and EMT progression. No significant differences in metastasis rates and EMT-related marker expression levels were observed between vehicle- and nicotine-treated mice. CONCLUSION: The results indicate that nicotine promotes cervical lymph node metastasis through regulating Ets1/Prx1/EMT signaling during OSCC pathogenesis; consequently, Prx1 may represent a potential target for the prevention and treatment of OSCC.

Nicotine suppresses apoptosis by regulating α7nAChR/Prx1 axis in oral precancerous lesions.

Nicotine, a tumor promoter in tobacco, can increase Peroxiredoxin (Prx1) and nicotinic acetylcholine receptors (nAChRs) in oral squamous cell carcinoma (OSCC). In the present study, we investigate the effects of nicotine in oral precancerous lesions focusing on apoptosis and nAChR/Prx1 signaling. We detected expression of Prx1, α3nAChR, α7nAChR, phosphorylation of mitogen-activated protein kinases (MAPK) and apoptosis in dysplastic oral keratinocyte (DOK) cells as well as in 4-nitroquinoline 1-oxide (4NQO) or 4NQO + nicotine - induced oral precancerous lesions in Prx1 wild-type (Prx1+/+) and Prx1 knockdown (Prx1+/-) mice. In DOK cells, Prx1 knockdown and blocking α7nAChR activated apoptosis, and nicotine increased the expression of Prx1, α3nAChR and α7nAChR, and inhibited MAPK activation. Moreover, nicotine suppressed apoptosis depending on Prx1 and α7nAChR in DOK cells. In animal bioassay, nicotine and Prx1 promoted growth of 4NQO-induced precancerous lesions in mouse tongue. 4NQO plus nicotine suppressed MAPK activation in Prx1 wild-type mice but not in Prx1 knockdown mice. Our data demonstrate that nicotine inhibits cell apoptosis and promotes the growth of oral precancerous lesions via regulating α7nAChR/Prx1 during carcinogenesis of OSCC.

Peroxiredoxin 1 has an anti-apoptotic role via apoptosis signal-regulating kinase 1 and p38 activation in mouse models with oral precancerous lesions.

Peroxiredoxin 1 (Prx1) is important in the protection of cells from oxidative damage and the regulation of cell proliferation and apoptosis. Prx1 is overexpressed in oral precancerous lesions of oral leukoplakia (OLK) and oral cancer; however, the association between Prx1 expression and OLK pathogenesis remains unknown. The present study investigated the role of Prx1 and its molecular mechanisms in oxidative stress-induced apoptosis during the pathogenesis of OLK. Wild-type and Prx1 knockout mice were treated with 50 µg/ml 4-nitroquinoline-1-oxide (4NQO) or 4NQO + H2O2 for 16 weeks to establish mouse models with tongue precancerous lesions. Apoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. The expression of Prx1, apoptosis signal-regulating kinase 1 (ASK1), phosphor-ASK1, p38 and phosphor-p38 was analyzed using immunohistochemical staining, and their mRNA expression levels were evaluated by reverse transcription quantitative polymerase chain reaction. The present results demonstrated that 4NQO or 4NQO + H2O2 induced the development of tongue precancerous lesions in Prx1 knockout and wild-type mice. Prx1 was overexpressed in tongue precancerous lesions compared with normal tongue mucosa. There was a significant decrease in the degree of moderate or severe epithelial dysplasia, and mild epithelial dysplasia was clearly elevated, in Prx1 knockout mice treated with 4NQO + H2O2 compared with wild-type mice treated with 4NQO + H2O2. Prx1 suppressed apoptosis and upregulated phosphor-ASK1 and phosphor-p38 expression in tongue precancerous lesions. The present results suggest that Prx1 suppresses oxidative stress-induced apoptosis via the ASK1/p38 signalling pathway in mouse tongue precancerous lesions. In conclusion, Prx1 and H2O2 have a coordination role in promoting the progression of tongue precancerous mucosa lesions. The present findings provide novel insight into Prx1 function and the mechanisms of Prx1 in OLK pathogenesis.

Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis.

Tobacco smoking is the major risk factor for oral squamous cell carcinoma (OSCC). Previously, we found that nicotine up-regulates peroxiredoxin 1 (Prx1), an important antioxidant enzyme, and nuclear factor kappa B (NFκB) in OSCC cells. However, the molecular mechanism of Prx1 in oral carcinogenesis remains obscure. To improve our understanding of the functional role of Prx1 during the cascade of tobacco-associated oral carcinogenesis, we characterized Prx1, NFκB, and epithelial-to-mesenchymal transition (EMT) markers including E-cadherin, vimentin and Snail in 30 primary oral tumors (15 from smokers with OSCC and 15 from non-smokers with OSCC) and 10 normal oral mucosa specimens from healthy individuals. The expression levels of Prx1, nuclear NFκB, vimentin and Snail were higher in the tumors from smokers with OSCC than in those from non-smokers with OSCC or the healthy controls. The expression levels of E-cadherin showed an opposite trend. Prx1 silencing suppressed the nicotine-induced EMT, cell invasion and migration in SCC15 cells in vitro. Furthermore, Prx1 activated the NFκB pathway in SCC15 cells. Prx1 might therefore play an oncogenic role in tobacco-related OSCC and thus serve as a target for chemopreventive and therapeutic interventions.

Peroxiredoxin 1 suppresses apoptosis via regulation of the apoptosis signal-regulating kinase 1 signaling pathway in human oral leukoplakia.

Peroxiredoxin 1 (Prx1) has a significant role in several malignant types of tumor. However, the role of Prx1 in oral leukoplakia (OLK) has remained to be elucidated. OLK is a common precancerous lesion of the oral mucosa that has a very high malignant transformation rate. The aim of the present study was to investigate the roles of Prx1, and its association with apoptosis signal-regulating kinase 1 (ASK1) and p38 in OLK. A total of 20 OLK samples and 10 normal oral mucosa samples were obtained from patients at the Beijing Stomatological Hospital (Beijing, China). The messenger RNA (mRNA) and protein expression levels of Prx1, ASK1 and p38 were determined by polymerase chain reaction and western blot analysis, respectively. Flow cytometry was used to detect cell apoptosis. The interaction between Prx1 and ASK1 was examined in H2O2-treated DOK cells by glutathione-S-transferase pull-down assays and by co-immunoprecipitation in vitro. Compared with those of the normal oral mucosa, the mRNA levels of Prx1, ASK1 and p38 were elevated in OLK tissues (P<0.05). The protein expression levels of Prx1, phosphorylated-ASK1 (p-ASK1) and p-p38 were also significantly enhanced in OLK tissues compared with those of the normal mucosa (P<0.05). In Prx1-knockdown DOK cells, ASK1 and p38 were activated, leading to enhanced levels of apoptosis in response to H2O2. No clear interaction between Prx1 and ASK1 was detected in H2O2-treated DOK cells. Prx1 was suggested to be involved in OLK pathogenesis by providing resistance against extracellular damages from oxidative stress via inhibition of the ASK1-induced apoptotic signaling pathway. Targeting Prx1 may provide a novel therapeutic strategy for the treatment of patients with OLK.