The application of metaverse in healthcare.

While metaverse is widely discussed, comprehension of its intricacies remains limited to a select few. Conceptually akin to a three-dimensional embodiment of the Internet, the metaverse facilitates simultaneous existence in both physical and virtual domains. Fundamentally, it embodies a visually immersive virtual environment, striving for authenticity, where individuals engage in real-world activities such as commerce, gaming, social interaction, and leisure pursuits. The global pandemic has accelerated digital innovations across diverse sectors. Beyond strides in telehealth, payment systems, remote monitoring, and secure data exchange, substantial advancements have been achieved in artificial intelligence (AI), virtual reality (VR), augmented reality (AR), and blockchain technologies. Nevertheless, the metaverse, in its nascent stage, continues to evolve, harboring significant potential for revolutionizing healthcare. Through integration with the Internet of Medical Devices, quantum computing, and robotics, the metaverse stands poised to redefine healthcare systems, offering enhancements in surgical precision and therapeutic modalities, thus promising profound transformations within the industry.

Advancements in brain-machine interfaces for application in the metaverse.

In recent years, with the shift of focus in metaverse research toward content exchange and social interaction, breaking through the current bottleneck of audio-visual media interaction has become an urgent issue. The use of brain-machine interfaces for sensory simulation is one of the proposed solutions. Currently, brain-machine interfaces have demonstrated irreplaceable potential as physiological signal acquisition tools in various fields within the metaverse. This study explores three application scenarios: generative art in the metaverse, serious gaming for healthcare in metaverse medicine, and brain-machine interface applications for facial expression synthesis in the virtual society of the metaverse. It investigates existing commercial products and patents (such as MindWave Mobile, GVS, and Galea), draws analogies with the development processes of network security and neurosecurity, bioethics and neuroethics, and discusses the challenges and potential issues that may arise when brain-machine interfaces mature and are widely applied. Furthermore, it looks ahead to the diverse possibilities of deep and varied applications of brain-machine interfaces in the metaverse in the future.

N6-Methyladenosine Modification of PTTG3P Contributes to Colorectal Cancer Proliferation via YAP1.

BACKGROUND: Long noncoding RNAs (lncRNAs) have emerged to have irreplaceable roles in the epigenetic regulation of cancer progression, but their biological functions in colorectal cancer (CRC) remain unclear. METHODS: LncRNA expression profiles in CRC tissue and their normal counterpart were explored. Through gain and loss of function approaches, the role of lncRNA PTTG3P was validated in relevant CRC cells and subcutaneous tumor model. The correlations of PTTG3P expression with clinical outcomes were assessed. RESULTS: PTTG3P was upregulated in CRC tissues and was closely correlated with unsatisfactory prognosis. PTTG3P facilitated glycolysis and proliferation, and the transcriptional regulator YAP1 was necessary for PTTG3P-induced proliferation. Mechanistically, the N6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify PTTG3P m6A methylation status and bind to it. IGF2BP2 knockdown partly recovered PTTG3P expression induced by METTL3, indicating that METTL3-regulated PTTG3P expression depended on the presence of IGF2BP2. Finally, rescue assays validated the critical role of the METTL3/PTTG3P/YAP1 axis on CRC proliferation. CONCLUSIONS: PTTG3P is an independent prognostic biomarker for CRC. The METTL3/PTTG3P/YAP1 axis promotes the progression of CRC and is a promising treatment target.

Hypoxia-induced PTTG3P contributes to colorectal cancer glycolysis and M2 phenotype of macrophage.

Long noncoding RNAs (lncRNAs) play critical factors in tumor progression and are ectopically expressed in malignant tumors. Until now, lncRNA pituitary tumor-transforming 3, pseudogene (PTTG3P) biological function in colorectal cancer (CRC) further needs to be clarified. qRT-PCR was used to measure the PTTG3P level and CCK-8, glucose uptake, lactate assay, adenosine triphosphate (ATP) assay, extracellular acidification rate (ECAR) assay, and xenograft mice model were adopted to evaluate the glycolysis and proliferation, and macrophage polarization were determined in CRC cells. Xenograft experiments were utilized to analyze tumor growth. Ectopic expression of PTTG3P was involved in CRC and related to dismal prognosis. Through gain- and loss-of-function approaches, PTTG3P enhanced cell proliferation and glycolysis through YAP1. Further, LDHA knockdown or glycolysis inhibitor (2-deoxyglucose (2-DG), 3-BG) recovered from PTTG3P-induced proliferation. And PTTG3P overexpression could facilitate M2 polarization of macrophages. Silenced PTTG3P decreased the level of inflammatory cytokines TNF-α, IL-1ß and IL-6, and low PTTG3P expression related with CD8+ T, NK, and TFH cell infiltration. Besides, hypoxia-inducible factor-1α (HIF1A) could increase PTTG3P expression by binding to the PTTG3P promoter region. Hypoxia-induced PTTG3P contributes to glycolysis and M2 phenotype of macrophage, which proposes a novel approach for clinical treatment.

LncRNA C9orf139 can regulate the growth of pancreatic cancer by mediating the miR-663a/Sox12 axis.

BACKGROUND: Recent studies have proved the important role of many oncogenic long non-coding RNAs (lncRNAs) in the progression of pancreatic cancer, but little is known about the mechanisms of tumor suppression in pancreatic cancer. AIM: To evaluate the function of tumor suppressor lncRNA C9orf139 in pancreatic cancer progression and to study the underlying mechanism. METHODS: We assigned 54 patients with pancreatic ductal adenocarcinoma treated at our hospital to the patient group and 30 normal subjects undergoing physical examination to the control group. RT-qPCR was used to measure the relative expression of C9orf139 in the tissue and serum of patients, in an attempt to investigate the prognostic value of C9orf139 in pancreatic cancer patients. The luciferase reporter gene assay was performed to determine the interaction between C9orf139 and miR-663a. The biological function of C9orf139 was assessed by in vitro assays and in vivo subcutaneous tumor formation tests in animal models. To figure out the molecular mechanism of C9orf139 to act on miR-663a/Sox12, RNA pull-down, Western blot assay, RNA immunoprecipitation assay, and co-immunoprecipitation assay were performed. RESULTS: C9orf139 level significantly increased in the tissue and serum of patients, which had clinical diagnostic value for pancreatic cancer. Patients with high C9orf139 expression had a higher risk of progressing to stage III + IV, lymph node metastasis, and poor differentiation. Cox regression analysis suggested that C9orf139, tumor-node-metastasis stage, and lymph node metastasis were independent prognostic factors in patients. The underlying mechanism of C9orf139 was that it promoted the growth of pancreatic cancer cells by modulating the miR-663a/Sox12 axis. CONCLUSION: C9orf139 is highly expressed in pancreatic cancer, qualified to be used as a potential diagnostic and prognostic marker for pancreatic cancer. Its promotion of pancreatic cancer cell growth is achieved by mediating the miR-663a/Sox12 axis.

Rab14 overexpression regulates gemcitabine sensitivity through regulation of Bcl-2 and mitochondrial function in pancreatic cancer.

Rab family protein Rab14 has been implicated in the development of human cancers. To date, its expression pattern, biological function, and potential mechanism in pancreatic cancer have not been explored. In this study, we analyzed Rab14 expression in 103 cases of pancreatic cancer tissues using immunohistochemistry (IHC) and found that Rab14 was overexpressed in 41/103 cases (39.8%). Rab14 overexpression correlated with the advanced stage. Moreover, elevated Rab14 levels indicated poor prognosis of patients with pancreatic cancers. We used BxPC-3 and Capan-2 respectively for plasmid and siRNA transfection. MTT and colony formation assays showed that Rab14 transfection increased cell proliferation and colony formation in BxPC-3 cells. Rab14 siRNA knockdown inhibits proliferation and colony formation ability in Capan-2 cell line. Cell cycle analysis showed that Rab14 facilitated cell cycle progression. Matrigel invasion assay showed that Rab14 promoted BxPC-3 cell invasion while its depletion inhibited Capan-2 cell invasion. In addition, MTT and AnnexinV/PI analysis demonstrated that overexpression of Rab14 reduced gemcitabine sensitivity which conversely was increased by Rab14 knockdown. We also demonstrated that Rab14 upregulated mitochondrial membrane potential (MMP) while its depletion downregulated MMP during gemcitabine treatment. In addition, western blotting revealed that Rab14 overexpression upregulated cyclin D1, cyclin A, cyclin E, p-Rb, and Bcl-2 and downregulated p21. Rab14 also downregulated caspase3, PARP cleavage, and cytochrome c release. In conclusion, our data indicated that Rab14 was overexpressed in pancreatic cancer and promotes growth and gemcitabine resistance, possibly through regulation of mitochondrial function and Bcl-2.

Association between alcohol consumption and colorectal cancer risk: a case-control study in the Han Chinese population.

Many epidemiologic studies have reported that alcohol is a risk factor for colorectal cancer. To further evaluate the association, we carried out a case-control study in the Han Chinese population. From February 2008 to February 2013, we carried out a hospital-based case-control study on colorectal cancer. Information was collected using a questionnaire. Cases were 310 patients with colorectal cancer; 620 healthy matched controls were also recruited. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals. Alcohol consumption was associated with increased colorectal cancer risk, but OR was significant only among heavy drinkers (OR=2.18, for ≥21 drinks/week). Colorectal cancer risk was 4.01-fold higher in heavy smokers (≥20 cigarettes/day) and heavy drinkers (≥21 drinks/week) in comparison with never smokers who consumed less than 7 drinks/week. The relationship was strengthened by stratified studies of sex. Among former drinkers, the excess of risk disappeared in those who had quit for at least 10 years (OR=0.86). Our study confirmed that heavy alcohol consumption was associated with an increasing risk of colorectal cancer; smoking modified this relationship, especially heavy smokers. Further data from large cohorts are desirable for conclusive confirmation.

Impact of PTEN IVS4 Polymorphism (rs3830675) on Cancer Susceptibility: An Updated Meta-analysis.

BACKGROUND/AIM: Phosphatase and tensin homolog (PTEN) acts as a tumor suppressor gene through the action of its phosphatase protein product. We performed a meta-analysis to evaluate their relationship. MATERIALS AND METHODS: A comprehensive database search was performed. Odds ratios (OR) with 95% confidence intervals (CI) were calculated to assess the association between PTEN IVS4 polymorphism and cancer. RESULTS: The meta-analysis indicated that PTEN IVS4 (-/-) genotype was significantly associated with the risk of cancer (OR=1.47, 95% CI=1.11-1.84), especially for digestive cancer (OR=1.67, 95% CI=1.28-2.18) compared to the (+/+) genotype. Moreover, the (-) allele of PTEN IVS4 polymorphism was also significantly associated with the risk of cancer (OR=1.27, 95% CI=1.14-1.41), especially for digestive cancer (OR=1.42, 95% CI=1.16-1.74) compared to the (+) allele. No significant association was observed between PTEN IVS4 (+/-) genotype and risk of cancer. CONCLUSION: PTEN IVS4 (-/-) genotype was significantly associated with increased risk of cancer especially for digestive tract cancer compared to the (+/+) genotype. A similar phenomenon was observed in the (-) allele of PTEN IVS4 polymorphism compared to the (+) allele and the recessive effect model.