Reactive oxygen species (ROS)‐mediated tumor catalytic therapy is typically hindered by gap junction proteins that form cell‐to‐cell channels to remove cytotoxic ROS, thereby protecting tumor cells from oxidative damage. In this work, a multifunctional nanozyme, FePGOGA, is designed and prepared by Fe(III)‐mediated oxidative polymerization (FeP), followed by glucose oxidase (GOx) and GAP19 peptides co‐loading through electrostatic and π–π interactions. The FePGOGA nanozyme exhibits excellent cascade peroxidase‐ and glutathione‐oxidase‐like activities that efficiently catalyze hydrogen peroxide conversion to hydroxyl radicals and convert reduced glutathione to oxidized glutathione disulfide. The loaded GOx starves the tumors and aggravates tumor oxidative stress through glucose decomposition, while GAP19 peptides block the hemichannels by inducing degradation of Cx43, thus increasing the accumulation of intracellular ROS, and decreasing the transport of intracellular glucose. Furthermore, the ROS reacts with primary amines of heat shock proteins to destroy their structure and function, enabling tumor photothermal therapy at the widely sought‐after mild temperature (mildPTT, ≤45 °C). In vivo experiments demonstrate the significant antitumor effectof FePGOGA on cal27 xenograft tumors under near‐infrared light irradiation. This study demonstrates the successful ablation of gap junction proteins to overcome resistance to ROS‐mediated therapy, providing a regulator to suppress tumor self‐preservation during tumor starvation, catalytic therapy, and mildPTT.
Objective Oral squamous cell carcinoma (OSCC) is one of the most common cancers, accounting for over 90% of malignant lesions in the oral cavity. Long non-coding RNAs play an important role in the development of OSCC. This study aimed to investigate the effects of lncRNA XIST on the malignant behaviors of OSCC cells and its possible molecular mechanisms. Methods Real-time quantitative PCR and Western blot were used to detect the RNA and protein level, respectively. CAL27 and SCC25 cells with the lowest expression level of XIST were used for further study. MTT, transwell assay, colony formation, and xenograft model were applied to examine the effect of XIST on the progression of OSCC. FISH assay was performed to investigate the co-location of XIST and miR-455-3p in OSCC cells. The bioinformatics analysis, luciferase, and RNA pull down assay were utilized to predict and verify the target genes of miR-455-3p. Results XIST was downregulated in OSCC tissues and cell lines. Overexpression of XIST inhibited the proliferation, migration, and invasion ability of OSCC cells. Bioinformatics analysis and luciferase reporter assay confirmed XIST could bind to miR-455-3p. Besides, miR-455-3p directly targeted BTG2 in OSCC cells. Rescue experiments further confirmed the positive interaction between miR-455-3p and XIST as well as between miR-455-3p and BTG2. Conclusion XIST was down-regulated in OSCC. XIST regulated the expression of BTG2 via sponging miR-455-3p. XIST/miR-455-3p/BTG2 signal axis inhibited the malignant progression of OSCC.
The disease of HNSCC ranks 6th among common malignancies, accounting for 5% of all cancer cases and 2%-3% of all cancer deaths (Ferlay et al., 2019). The incidence, metastatic and mortality rates of HNSCC have increased rapidly in recent years. More than 550,000 people worldwide are diagnosed with HNSCC each year, and more than 380,000 die from the disease (Vermorken & Specenier, 2010).Today, we rely on imaging examinations such as magnetic resonance imaging (MRI), computed tomography (CT), positron emission computed tomography (PET) (Jorgensen et al., 2019), histological analysis of primary tumour biopsy and fine needle aspirate (FNA)
Oral squamous cell carcinoma (OSCC) is a common cancer with high recurrence, metastasis rates and poor prognosis. Circular RNAs (circRNAs) take part in regulating OSCC. Herein, we examined the role of circ_0008068 in OSCC. The circ_0008068, Katanin p60 ATPase-containing subunit A-like 1 (KATNAL1) mRNA, microRNA-153-3p (miR-153-3p) and acylgycerol kinase (AGK) contents were indicated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Moreover, in vitro and in vivo assays were conducted to scrutinize the effects of circ_0008068 on OSCC. Additionally, the contact between miR-153-3p and circ_0008068 or AGK was assessed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Thereafter, we found that the appearance of circ_0008068 and AGK was increased, and miR-153-3p content was diminished in OSCC. Circ_0008068 lack subdued cell proliferation, migration, invasion, tube formation and glycolysis metabolism, but stimulated cell apoptosis in OSCC. In addition, circ_0008068 bound to miR-153-3p to modulate the expression of its target AGK. Besides, miR-153-3p was validated to act as a tumor suppressor in OSCC tumorigenesis by suppressing AGK. Additionally, circ_0008068 knockdown also attenuated tumor growth in nude mice. In all, circ_0008068 expedited the growth of OSCC by miR-153-3p/AGK axis. Abbreviations: OSCC: Oral squamous cell carcinoma; AGK: Acylgycerol kinase; CircRNA: Circular RNA; KATNAL1: Katanin p60 ATPase-containing subunit A-like 1; qRT-PCR: Quantitative real-time polymerase chain reaction; miRNAs/miRs: MicroRNAs; RIP: RNA immunoprecipitation; 3′UTR3’: -untranslated region; HK2: Hexokinase 2; LDHA Lactate dehydrogenase A; IHC: Immunohistochemistry; CCK8: Cell counting kit-8; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase
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