Polycystic ovarian syndrome (PCOS) is a common heterogeneous reproductive endocrine metabolic disorder in women of reproductive age characterized by clinical and biochemical hyperandrogenemia, ovulation disorders, and polycystic ovarian morphology. Ferroptosis is a novel type of cell death driven by iron accumulation and lipid peroxidation. Ferroptosis plays a role in maintaining redox balance, iron metabolism, lipid metabolism, amino acid metabolism, mitochondrial activity, and many other signaling pathways linked to diseases. Iron overload is closely related to insulin resistance, decreased glucose tolerance, and the occurrence of diabetes mellitus. There is limited research on the role of ferroptosis in PCOS. Patients with PCOS have elevated levels of ferritin and increased reactive oxygen species in ovarian GCs. Studying ferroptosis in PCOS patients is highly important for achieving personalized treatment. This article reviews the progress of research on ferroptosis in PCOS, introduces the potential connections between iron metabolism abnormalities and oxidative stress-mediated PCOS, and provides a theoretical basis for diagnosing and treating PCOS.

SMALL AUXIN UP RNAs (SAURs), the largest family of early auxin response genes, plays crucial roles in multiple processes, including cell expansion, leaf growth and senescence, auxin transport, tropic growth and so on. Although the rice SAUR gene family was identified in 2006, it is necessary to identify the rice SAUR gene due to the imperfection of its analysis methods. In this study, a total of 60 OsSAURs (including two pseudogenes) distributed on 10 chromosomes were identified in rice (Oryza sativa). Bioinformatics tools were used to systematically analyze the physicochemical properties, subcellular localization, motif compositions, chromosomal location, gene duplication, evolutionary relationships, auxin-responsive cis-elements of the OsSAURs. In addition, the expression profiles obtained from microarray data analysis showed that OsSAUR genes had different expression patterns in different tissues and responded to auxin treatment, indicating functional differences among members of OsSAUR gene family. In a word, this study provides basic information for SAUR gene family of rice and lays a foundation for further study on the role of SAUR in rice growth and development.

Introduction The objective of the present study was to identify gene expression in peripheral blood by a real-time polymerase chain reaction (PCR) technique in patients who have lung carcinoma. Material and methods Peripheral blood samples of patients with non-small cell and small cell lung cancer were collected. Target genes included survivin, CK7, ASH1, HMGB3, L587S, and CLCA2. β-Actin was the reference gene. If the mean CT (threshold cycle) value for a target gene is ≥40, the gene expression is considered undetectable. Results Fifty patients with lung carcinoma were included and 30 healthy controls. Out of the six genes, survivin showed 26.8 times fold change as compared to controls; ASH1 and L587S were 0.54 and 0.06, respectively; and HMGB3, CLCA2, and CK7 had non-significant fold change in comparison to controls. The overall detection rate of the six target genes examined in lung cancer was 84%, with 42 out of 50 patients testing positive. Higher stages and ASH1 (p = 0.031), CK7 (p = <0.001), and HMGB3, p = 0.011 were associated significantly. CLCA2 had higher expression in patients without adrenal metastases (p = 0.044). Conclusions Lifestyle and geographical variation might be a probable cause of variable gene expression as compared to other studies. However, further research is needed to determine the clinical implication of these markers, especially in larger groups of early-stage patients.

OBJECTIVE: To evaluate the expression of Ribosomal S6 kinase 4 (RSK4) protein in non-small cell lung cancer (NSCLC) tissues and adjacent non-tumor tissues, and to elucidate its correlation with clinicopathological features of NSCLC.
METHODS: We analyzed 100 NSCLC patients treated at the Second Affiliated Hospital of Zhejiang University School of Medicine from June 2020 to June 2022. Patient demographics and clinical data, including gender, age, history of diabetes, tumor location, degree of tumor differentiation, lymph node metastasis, and clinical stage, were collected. RSK4 protein expression was assessed in tissue samples via immunohistochemical staining.
RESULTS: RSK4 protein was positively expressed in 35.00% of cancerous tissues, significantly lower than the 69.00% observed in adjacent non-tumor tissues (P < 0.05). Patients with lower tumor differentiation, advanced Tumor Node Metastasis (TNM) stages, and lymph node metastases showed significantly reduced RSK4 expression compared to those with higher differentiation, earlier TNM stages, and no lymph node metastases (all P < 0.05). Cox regression analysis indicated that TNM stage, low differentiation, and lymph node metastases significantly influenced RSK4 expression (all P < 0.05). Survival analysis revealed a higher positive prognosis survival rate of 74.29% (26/35) among patients with positive RSK4 expression, versus 53.85% (35/65) in those with negative expression (P < 0.05). Spearman correlation analysis demonstrated a significant positive correlation of RSK4 expression with TNM stage, lymph node metastasis, and patient prognosis (all P < 0.05).
CONCLUSIONS: Positive RSK4 expression in NSCLC tissues is significantly correlated with advanced cancer stage, poor differentiation, and presence of lymph node metastasis, suggesting a potential tumor suppressor role for RSK4 in NSCLC. This association underscores its prognostic relevance in NSCLC patients.

Long non-coding RNAs (lncRNAs), defined as RNA molecules exceeding 200 nucleotides in length, have been implicated in the regulation of various biological processes and the progression of tumors. Among them, LINC00518, a recently identified lncRNA encoded by a gene located on chromosome 6p24.3, consists of three exons and is predicted to positively regulate the expression of specific genes. LINC00518 has emerged as a key oncogenic lncRNA in multiple cancer types. It exerts its tumor-promoting effects by modulating the expression of several target genes, primarily through acting as a sponge for microRNAs (miRNAs). Additionally, LINC00518 influences critical signaling pathways, including the Wnt/β-catenin, JAK/STAT, and integrin β3/FAK pathways. Elevated levels of LINC00518 in tumor tissues are associated with increased tumor size, advanced clinical stage, metastasis, and poor survival prognosis. This review provides a comprehensive summary of the genetic characteristics, expression patterns, biological functions, and underlying mechanisms of LINC00518 in human diseases.

Melanoma antigen gene (MAGE) families are cancer-testis genes that normally show expression in the testes. However, their expressions have been linked with various types of human cancers, including BC. Therefore, the primary purposes of the present research were to assess the expression of MAGE-A, -B, and -C genes in Saudi female patients with BC and determine their regulation via the epigenetic mechanism. Ten BC samples were analyzed for the expression levels of nine MAGE-A genes, six MAGE-B genes, and three MAGE-C genes using the RT-PCR technique. All 18 evaluated genes except for MAGE-A1, -A3, -A4, and -B5 showed weak band expressions in some BC specimens. MAGE-A6 and -B2 were expressed in 40 % of the BC tissue samples, and MAGE-A9, -A10, and -B6 were expressed in 30 %. The lowest expression levels were found for MAGE-A11, -B1, -B3, -B4, -C1, and -C2 in 10 % of the BC specimens and for MAGE-A9,--B2, and --C3 in 20 % of the samples. The most frequently expressed gene was MAGE-A8 (found in 70 % of the BC samples), which suggests that it may serve as - a marker for screening of BC. In vitro treatment, the 5-aza-2\'-deoxycytidine agent led to a significant rise in mRNA expressions for all tested genes related to the MAGE-A family, except for MAGE-A10. By contrast, among the genes in the MAGE-B and -C families, only MAGE-B1 and -C2 exhibited detectable mRNA expression levels after treatment.

YEATS domain containing 2 (YEATS2), it may function as a proto-oncogene. This study aims to investigate if YEATS2 correlates with prognosis in hepatocellular carcinoma. The prognostic landscape of YEATS2 and its relationship with expression in hepatocellular carcinoma were deciphered with public databases, RT-qPCR and western-blot in tissue samples. The expression profiling and prognostic value of YEATS2 were explored using UALCAN, TIMER, OncoLnc database. Transcription and survival analyses of YEATS2 in hepatocellular carcinoma were investigated with cBioPortal database. The STRING database was explored to identify molecular functions and signaling pathways downstream of YEATS2. YEATS2 expression was significantly higher in hepatocellular carcinoma compared with adjacent non-malignant tissues. Promoter methylation of YEATS2 exhibited different patterns in hepatocellular carcinoma. High expression of YEATS2 was associated with poorer survival. Mechanistically, YEATS2 was involved in mediating multiple biological processes including morphogenesis and migration.

Mango is a popular tropical fruit that requires quarantine hot water treatment (QHWT) for postharvest sanitation, which can cause abiotic stress. Plants have various defense mechanisms to cope with stress; miRNAs mainly regulate the expression of these defense responses. Proteins involved in the biogenesis of miRNAs include DICER-like (DCL), ARGONAUTE (AGO), HYPONASTIC LEAVES 1 (HYL1), SERRATE (SE), HUA ENHANCER1 (HEN1), HASTY (HST), and HEAT-SHOCK PROTEIN 90 (HSP90), among others. According to our analysis, the mango genome contains five DCL, thirteen AGO, six HYL, two SE, one HEN1, one HST, and five putative HSP90 genes. Gene structure prediction and domain identification indicate that sequences contain key domains for their respective gene families, including the RNase III domain in DCL and PAZ and PIWI domains for AGOs. In addition, phylogenetic analysis indicates the formation of clades that include the mango sequences and their respective orthologs in other flowering plant species, supporting the idea these are functional orthologs. The analysis of cis-regulatory elements of these genes allowed the identification of MYB, ABRE, GARE, MYC, and MeJA-responsive elements involved in stress responses. Gene expression analysis showed that most genes are induced between 3 to 6 h after QHWT, supporting the early role of miRNAs in stress response. Interestingly, our results suggest that mango rapidly induces the production of miRNAs after heat stress. This research will enable us to investigate further the regulation of gene expression and its effects on commercially cultivated fruits, such as mango, while maintaining sanitary standards.

BACKGROUND: Background: Genome-wide association studies (GWAS) have identified hundreds of genetic variants associated with cancer risk. GWAS data are important for cancer prevention and understanding the underlying mechanisms of cancer.
OBJECTIVE: This study aimed to investigate the genetic association between different types of cancer using GWAS data and a bioinformatics approach.
RESULTS: The significant GWAS variants associated with more than one cancer type were identified. Common linkage disequilibrium (LD) variants between different types of cancer were identified by 1000 genomes phase 3 LD data. Haplotype blocks were identified by analyzing 1000 Genomes phase 3 genotyping data in the GWAS populations. Subsequent analyses included functional SNP analyses and TCGA gene expression. The results associated with significant GWAS variants (P<5E-8) showed the following haplotype associations in European population: GT rs4808075-rs8170 haplotype on BABAM1 with breast and ovarian cancers, GC rs16857609-rs11693806 haplotype on DIRC3 with breast and thyroid cancers, GCG rs380286-rs401681-rs31487 haplotype on CLPTM1L with skin and lung cancers, GGG rs4430796-rs11651052-rs11263763 haplotype on HNF1B with prostate and endometrial cancers, and GT rs10505477-rs6983267 haplotype on CASC8 associated with colorectal and prostate cancers. All these genes had significantly different expressions in tumor tissues (P<1E-3). In addition, the rs11693806 variant is located in the hsa-miR-873-5p binding site and has an enhancing effect on the hsa-miR-873-5p:DIRC3 interaction.
CONCLUSIONS: These novel haplotype structures and miRNA:lncRNA interactions are important for understanding the common genetic link between cancers. These results can potentially be used in genetic panels.

UNASSIGNED: Glycosylphosphatidylinositol (GPI)-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) plays a crucial role in fatty acid metabolism, which is involved in the progression of colorectal cancer (CRC). The aim of this study was to determine the expressional variations of GPIHBP1 in CRC at different stages and to verify whether this protein affects the shaping of the immune microenvironment of cancer cells.
UNASSIGNED: Variations of GPIHBP1 messenger RNA (mRNA) levels were first analysed using The Cancer Genome Atlas (TCGA) database. Protein levels of GPIHBP1 in cancer nest cells, stromal cells or surrounding normal tissues from 68 patients with CRC were checked by immunohistochemistry. Infiltration of immune cells such as macrophages, myeloid-derived suppressor cells (MDSCs), CD8+ and CD56+ cells was parallelly stained in the same tissues. Ectopic GPIHBP1 expressed colonic tumour cells were transplanted into the back of mice. Tumour growth and immune cell infiltrations were also observed.
UNASSIGNED: Compared with those in healthy tissues, GPIHBP1 mRNA and protein levels decreased in the patients with CRC at Dukes A-B stage but gradually increased in the patients at Dukes C-D stage. GPIHBP1 in foci or stroma was positively correlated with recruited macrophages or MDSCs and negatively correlated with recruited CD8+, CD56+ or granzyme+ cells. The mice injected with GPIHBP1 overexpression cells bore large tumours. Histological analysis confirmed the infiltration of many macrophages and MDSCs but less CD8+ T or CD56+ cells.
UNASSIGNED: The increased expression of GPIHBP1 is involved in the progression of CRC. High GPIHBP1 level of advanced CRC indicates efficient immune evasion in tumour microenvironment.