Quality of life assessment in patients with alopecia areata and androgenetic alopecia in the People’s Republic of China Min Zhang,1 Nan Zhang2 1Department of Dermatology, 2Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, People’s Republic of China Introduction: In medical terms, alopecia is considered a relatively mild dermatological condition that nevertheless is a serious condition, but it causes major depression in many sufferers. Alopecia areata (AA) and androgenetic alopecia (AGA) are the main types of hair loss. This study assessed the quality of life (QoL) of Chinese patients with AA and AGA using the Dermatology Life Quality Index (DLQI) questionnaire.Methods: A total of 178 AA and AGA patients were enrolled in this study, and DLQI was used to evaluate the QoL of the patients. The DLQI used 10 items regarding symptoms and feelings, daily activities, leisure, work and school, personal relationships, and treatment as dimensions of life. Each was scored on a 0–3 scale. The total DLQI score equaled 0–30; higher scores showed greater impact on QoL.Results: The DLQI scores of the 178 patients ranged from 0 to 28, with a mean score of 6.3. Higher DLQI scores were reported by younger patients (P12 months (P<0.05). The DLQI score of AA patients was significantly higher than that of AGA patients (P12 months, and AA. Both AA and AGA moderately affected the QoL of the patients not only in physiological aspects but also in their emotional and social aspects. The bio-psycho-social aspects of disease need to be addressed in patients with AA and AGA, even though these conditions are not life-threatening. Keywords: alopecia, quality of life, People’s Republic of China

N6-methyl-adenosine(m6A) modification emerges as an abundant and dynamic regulation throughout the Eukaryotic transcriptome. Dysregulation of the m6A regulators has increasingly been found in many neoplasms. It is reasonable to believe that m6A changes the fate of cancer cells and subsequently affected all aspects of cancer progression. In view of the context-dependent role of m6A modification, we emphasize a dual effect of m6A in a particular tumor model, that is, m6A plays a promoting role or a suppressing role in different stages of cancer. This novel sight is compared to the older view that a particular m6A regulator acts as a consistent role in cancer progression.

Lung cancer remains one of the major causes of cancer-related death globally. Recent studies have shown that aberrant m⁶A levels caused by METTL3 are involved in the malignant progression of various tumors, including lung cancer. The m⁶A modification, the most abundant RNA chemical modification, regulates RNA stabilization, splicing, translation, decay, and nuclear export. The methyltransferase complex plays a key role in the occurrence and development of many tumors by installing m⁶A modification. In this complex, METTL3 is the first identified methyltransferase, which is also the major catalytic enzyme. Recent findings have revealed that METTL3 is remarkably associated with different aspects of lung cancer progression, influencing the prognosis of patients. In this review, we will focus on the underlying mechanism of METT3 in lung cancer and predict the future work and potential clinical application of targeting METTL3 for lung cancer therapy.

Background: N6-methyladenosine (m6A) is a dynamic and reversible internal RNA structure of eukaryotic mRNA. YTH domain family 2 (YTHDF2), an m6A-specific reader YTH domain family, plays fundamental roles in several types of cancer. However, the function of YTHDF2 in lung squamous cell carcinoma (LUSC) remains elusive. Methods: The knockdown and overexpression of YTHDF2 in LUSC cells were conducted to detect the biological characteristics of YTHDF2. In vivo assays, the role of YTHDF2 in tumor growth was further uncovered. In vitro assays, YTHDF2 was confirmed to be involved in activating the mTOR/AKT signaling and YTHDF2 overexpression induced the EMT process in LUSC. Clinically, immunohistochemical staining revealed the relationship between YTHDF2 expression levels and the clinicopathological characteristics of lung squamous cell carcinoma patients. Moreover, quantitative PCR (qPCR), western blot, CCK8 assay, transwell assay, and wound-healing assay were used to detect the expression level and function of YTHDF2 under hypoxia exposure in LUSC cells. Results: The results showed that hypoxia-mediated YTHDF2 overexpression promotes cell proliferation and invasion by activating the mTOR/AKT axis, and YTHDF2 overexpression induces the EMT process in LUSC. Moreover, YTHDF2 is closely associated with pN (pN– 37.0%, pN + 73.9%; P = 0.002) and pTNM stage (pI 50.0%, PII 43.3%, pIIIa 80.6%; P = 0.007), ultimately resulting in poor survival for LUSC patients. Conclusion: In brief, the results highlight high-YTHDF2 expression predicted a worse prognosis of LUSC, while hypoxia-mediated YTHDF2 overexpression promotes lung squamous cell carcinoma progression by activation of the mTOR/AKT signaling pathway.

A DNA walker powered by endogenous enzymes is constructed. It performs automatic walking in living cells and can detect the uracil-DNA glycosylase activity in situ.

N6-methyladenosine (m⁶A) is the most prevalent reversible modification in eukaryotic mRNA, and it plays a critical role in tumor progression. The purpose of this study was to investigate the function and regulatory mechanisms of the methyltransferase METTL3 in renal cell carcinoma (RCC). METTL3 expression was upregulated and predicted a poor prognosis in patients with advanced RCC. METTL3 facilitated the proliferation, migration, and invasion of RCC cells, depending on its methylase activity. METTL3 positively regulated the expression of PLOD2, and both genes were triggered under prolonged hypoxia. Mechanistically, hypoxia-induced the binding of HIF-1α to the METTL3 promoter, which enhanced its transcriptional activity. METTL3-mediated m⁶A modifications of PLOD2 mRNA at 3’UTR region, promoting the translation of PLOD2 protein. Furthermore, silencing METTL3 impaired RCC progression in vitro. In vivo, administration of highly potent and selective METTL3 inhibitor STM2457 showed anti-tumor effects, whereas AAV9-mediated re-transduction of PLOD2 largely abolished the above phenomenon in a subcutaneous mouse model. These findings reveal that hypoxia and HIF-driven METTL3 transcription promote RCC progression by increasing PLOD2 expression in an m⁶A-dependent manner, suggesting that METTL3 may serve as a novel pharmaceutical intervention for RCC.