Challenges and Remedies to Privacy and Security in AIGC: Exploring the Potential of Privacy Computing, Blockchain, and Beyond

Artificial Intelligence Generated Content (AIGC) is one of the latest achievements in AI development. The content generated by related applications, such as text, images and audio, has sparked a heated discussion. Various derived AIGC applications are also gradually entering all walks of life, bringing unimaginable impact to people's daily lives. However, the rapid development of such generative tools has also raised concerns about privacy and security issues, and even copyright issues in AIGC. We note that advanced technologies such as blockchain and privacy computing can be combined with AIGC tools, but no work has yet been done to investigate their relevance and prospect in a systematic and detailed way. Therefore it is necessary to investigate how they can be used to protect the privacy and security of data in AIGC by fully exploring the aforementioned technologies. In this paper, we first systematically review the concept, classification and underlying technologies of AIGC. Then, we discuss the privacy and security challenges faced by AIGC from multiple perspectives and purposefully list the countermeasures that currently exist. We hope our survey will help researchers and industry to build a more secure and robust AIGC system.Comment: 43 pages, 10 figure

NMI inhibits cancer stem cell traits by downregulating hTERT in breast cancer.

N-myc and STAT interactor (NMI) has been proved to bind to different transcription factors to regulate a variety of signaling mechanisms including DNA damage, cell cycle and epithelial-mesenchymal transition. However, the role of NMI in the regulation of cancer stem cells (CSCs) remains poorly understood. In this study, we investigated the regulation of NMI on CSCs traits in breast cancer and uncovered the underlying molecular mechanisms. We found that NMI was lowly expressed in breast cancer stem cells (BCSCs)-enriched populations. Knockdown of NMI promoted CSCs traits while its overexpression inhibited CSCs traits, including the expression of CSC-related markers, the number of CD44+CD24- cell populations and the ability of mammospheres formation. We also found that NMI-mediated regulation of BCSCs traits was at least partially realized through the modulation of hTERT signaling. NMI knockdown upregulated hTERT expression while its overexpression downregulated hTERT in breast cancer cells, and the changes in CSCs traits and cell invasion ability mediated by NMI were rescued by hTERT. The in vivo study also validated that NMI knockdown promoted breast cancer growth by upregulating hTERT signaling in a mouse model. Moreover, further analyses for the clinical samples demonstrated that NMI expression was negatively correlated with hTERT expression and the low NMI/high hTERT expression was associated with the worse status of clinical TNM stages in breast cancer patients. Furthermore, we demonstrated that the interaction of YY1 protein with NMI and its involvement in NMI-mediated transcriptional regulation of hTERT in breast cancer cells. Collectively, our results provide new insights into understanding the regulatory mechanism of CSCs and suggest that the NMI-YY1-hTERT signaling axis may be a potential therapeutic target for breast cancers

BPTF promotes tumor growth and predicts poor prognosis in lung adenocarcinomas.

BPTF, a subunit of NURF, is well known to be involved in the development of eukaryotic cell, but little is known about its roles in cancers, especially in non-small-cell lung cancer (NSCLC). Here we showed that BPTF was specifically overexpressed in NSCLC cell lines and lung adenocarcinoma tissues. Knockdown of BPTF by siRNA significantly inhibited cell proliferation, induced cell apoptosis and arrested cell cycle progress from G1 to S phase. We also found that BPTF knockdown downregulated the expression of the phosphorylated Erk1/2, PI3K and Akt proteins and induced the cleavage of caspase-8, caspase-7 and PARP proteins, thereby inhibiting the MAPK and PI3K/AKT signaling and activating apoptotic pathway. BPTF knockdown by siRNA also upregulated the cell cycle inhibitors such as p21 and p18 but inhibited the expression of cyclin D, phospho-Rb and phospho-cdc2 in lung cancer cells. Moreover, BPTF knockdown by its specific shRNA inhibited lung cancer growth in vivo in the xenografts of A549 cells accompanied by the suppression of VEGF, p-Erk and p-Akt expression. Immunohistochemical assay for tumor tissue microarrays of lung tumor tissues showed that BPTF overexpression predicted a poor prognosis in the patients with lung adenocarcinomas. Therefore, our data indicate that BPTF plays an essential role in cell growth and survival by targeting multiply signaling pathways in human lung cancers

KMT2A promotes melanoma cell growth by targeting hTERT signaling pathway.

Melanoma is an aggressive cutaneous malignancy, illuminating the exact mechanisms and finding novel therapeutic targets are urgently needed. In this study, we identified KMT2A as a potential target, which promoted the growth of human melanoma cells. KMT2A knockdown significantly inhibited cell viability and cell migration and induced apoptosis, whereas KMT2A overexpression effectively promoted cell proliferation in various melanoma cell lines. Further study showed that KMT2A regulated melanoma cell growth by targeting the hTERT-dependent signal pathway. Knockdown of KMT2A markedly inhibited the promoter activity and expression of hTERT, and hTERT overexpression rescued the viability inhibition caused by KMT2A knockdown. Moreover, KMT2A knockdown suppressed tumorsphere formation and the expression of cancer stem cell markers, which was also reversed by hTERT overexpression. In addition, the results from a xenograft mouse model confirmed that KMT2A promoted melanoma growth via hTERT signaling. Finally, analyses of clinical samples demonstrated that the expression of KMT2A and hTERT were positively correlated in melanoma tumor tissues, and KMT2A high expression predicted poor prognosis in melanoma patients. Collectively, our results indicate that KMT2A promotes melanoma growth by activating the hTERT signaling, suggesting that the KMT2A/hTERT signaling pathway may be a potential therapeutic target for melanoma

Ku80 cooperates with CBP to promote COX-2 expression and tumor growth.

Cyclooxygenase-2 (COX-2) plays an important role in lung cancer development and progression. Using streptavidin-agarose pulldown and proteomics assay, we identified and validated Ku80, a dimer of Ku participating in the repair of broken DNA double strands, as a new binding protein of the COX-2 gene promoter. Overexpression of Ku80 up-regulated COX-2 promoter activation and COX-2 expression in lung cancer cells. Silencing of Ku80 by siRNA down-regulated COX-2 expression and inhibited tumor cell growth in vitro and in a xenograft mouse model. Ku80 knockdown suppressed phosphorylation of ERK, resulting in an inactivation of the MAPK pathway. Moreover, CBP, a transcription co-activator, interacted with and acetylated Ku80 to co-regulate the activation of COX-2 promoter. Overexpression of CBP increased Ku80 acetylation, thereby promoting COX-2 expression and cell growth. Suppression of CBP by a CBP-specific inhibitor or siRNA inhibited COX-2 expression as well as tumor cell growth. Tissue microarray immunohistochemical analysis of lung adenocarcinomas revealed a strong positive correlation between levels of Ku80 and COX-2 and clinicopathologic variables. Overexpression of Ku80 was associated with poor prognosis in patients with lung cancers. We conclude that Ku80 promotes COX-2 expression and tumor growth and is a potential therapeutic target in lung cancer

An instrument to measure atrial fibrillation knowledge in Chinese patients: validation of the Jessa Atrial fibrillation Knowledge Questionnaire

Background: There is no validated tool to assess patients’ knowledge of oral anticoagulant therapy in atrial fibrillation in China.Methods: Using a standard translation program, the Jessa Atrial fibrillation Knowledge Questionnaire (JAKQ) was translated into Chinese. The reliability of the JAKQ was assessed by internal consistency (Cronbach’s α coefficient), repeatability (test-retest reliability), and sensitivity tests. Effectiveness was assessed by hypothesizing that a lower JAKQ score was a risk factor for bleeding. A total of 447 patients with atrial fibrillation (AF) who were hospitalized between July 2019 and December 2021 were studied and followed up. Participants were followed up 1, 3, 6, and 12 months after enrollment. Bleeding during follow-up was recorded. Data were obtained from hospital databases and telephone follow-up.Result: A total of 447 patients with AF completed JAKQ. The mean age of patients was 67.7 ± 10.2 years. The median JAKQ score was 31.3% (12.5–43.8). The Cronbach’s α coefficient of JAKQ was 0.616–0.637, and the test-retest reliability value was 0.902 (p < 0.001). Multivariate logistic regression showed that the higher knowledge level of AF was associated with secondary education or above, an income of more than 2000 yuan, and a history of AF of more than 1 year. Bleeding was associated with a lower JAKQ score, hypertension, and a history of bleeding. Non-bleeding patients on VKA had a better understanding of how often INR should be monitored and what to do if an OAC dose was missed.Conclusion: The Chinese version of JAKQ shows good reliability and validity, indicating that it is a valuable tool for AF and oral anticoagulation (OAC) knowledge assessment. It can be used in clinical practice to guide educational activities and improve the effectiveness and safety of treatment. It was shown that Chinese patients with AF have insufficient knowledge about AF and OAC. Lower JAKQ scores are associated with bleeding, so targeted education is necessary. Targeted educational efforts should focus on patients recently diagnosed with AF and those with lower formal education and income