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The Golgi apparatus is a membrane‐bound organelle that functions as a central role in the secretory pathway. Since the discovery of the Golgi apparatus, its structure and function have attracted ever‐increasing attention from researchers. Recently, it has been demonstrated that metal ions are necessary for the Golgi apparatus to maintain its proper structure and functions. Given that metal ions play an important role in various biological processes, their abnormal homeostasis is related to many diseases. Therefore, in this paper, we reviewed the uptake and release mechanisms of the Golgi apparatus Ca2+, Cu, and Zn2+. Furthermore, we describe the diseases associated with Golgi apparatus Ca2+, Cu, and Zn2+ imbalance. [ABSTRACT FROM AUTHOR]

The organelle of eukaryotes is a finely regulated system. Once disturbed, it activates the specific autoregulatory systems, namely, organelle autoregulation. Among which, the Golgi stress response accounts for one. When the abundance and capacity of the Golgi apparatus are insufficient compared with cellular demand, the Golgi stress response is activated to enhance the function of the Golgi apparatus. Although the molecular mechanism of the Golgi stress response has not been well characterized yet, it seems to be an important part of the mammalian stress response. In this review, we discuss the current status of research on the six pathways of the mammalian Golgi stress response (the TFE3, heat shock protein 47, CREB3, E26 transformation specific, proteoglycan, and mucin pathways), which regulate the general function of the Golgi apparatus, anti‐apoptosis, pro‐apoptosis, proteoglycan glycosylation, and mucin glycosylation, respectively. [ABSTRACT FROM AUTHOR]

A recent study suggests that ribosome MARylation in cancers maintains proteostasis by reducing protein synthesis and preventing toxic protein aggregation. Mechanistically, NMNAT‐2 is a cytosolic NAD+ synthase that supports the catalytic activity of PARP‐16, which mediates ribosomal proteins MARylation. Ribosomal protein MARylation regulates polysomes assembly or function through the 3′‐untranslated region (3′‐UTR) stem‐loop secondary structures in mRNAs, resulting in reduced protein synthesis and preventing toxic protein aggregation, thus supporting the growth of cancer cells during accelerated cell growth. When PARP‐16 or NMNAT‐2 is deleted, the stem‐loop element in the 3′‐UTRs of mRNAs increases polysome loading, enhances protein synthesis, promotes toxic protein aggregation, leading to inhibited cancer cell growth. Collectively, ribosome MARylation provides us with an exciting and scientific direction for us to understand cancers. [ABSTRACT FROM AUTHOR]

In recent years, circular RNAs have been shown to serve as essential regulators in several human cancers. Nevertheless, the function and mechanism of CircRNA in cervical cancer remain elusive. In the present study, we showed that hsa_circRNA_101996 was highly expressed in cervical cancer tissues compared with matched normal tissues by bioinformatics analysis. We showed that the expression level of hsa_circRNA_101996 in cervical cancer tissues was positively correlated with TNM stage, tumor size, and lymph node metastasis. Moreover, higher levels of hsa_circRNA_101996 were related to poor outcomes of cervical cancer patients. We found that knockdown of hsa_circRNA_101996 significantly inhibited the proliferation, cell cycle, migration, and invasion of cervical cancer cells. Mechanistically, we demonstrated that hsa_circRNA_101996 served as a sponge of miR‐8075, which targeted TPX2 in cervical cancer cells. We showed that miR‐8075 that was downregulated in cervical cancer tissues repressed cervical cancer cell proliferation, migration, and invasion. Furthermore, we validated that upregulation of TPX2 by hsa_circRNA_101996‐mediated inhibition of miR‐8075 contributed to cervical cancer proliferation, migration, and invasion. Taken together, our findings revealed a novel mechanism that hsa_circRNA_101996‐miR‐8075‐TPX2 network promoted cervical cancer progression. [ABSTRACT FROM AUTHOR]

N6‐methyladenosine (m6A) is one of the most common internal modifications in messenger RNA, which is necessary for cell physiological activities. A recent study shows that during mammalian hematopoietic development, loss of m6A modification leads to the aberrant production of double‐stranded RNA, which results in the abnormal activation of innate immune response, and ultimately leads to hematopoietic failure. Accordingly, m6A modification provide us an attractive direction for us to understand mammalian hematopoietic development and innate immune response. [ABSTRACT FROM AUTHOR]

Objective The objective of this study was to determine the levels of thrombospondin-1 (TSP-1), transforming growth factor-β1 (TGF-β1) and nuclear factor kappaβ (NF-κβ) in polycystic ovarian syndrome (PCOS) patients with and without insulin resistance and after treatment with cyproterone acetate/ethinyloestradiol with or without concomitant metformin. Design Prospective. Patients Patients with PCOS and healthy women were recruited. Patients were subdivided into obese and nonobese based on body mass index. Patients with PCOS were also grouped according to homoeostasis model assessment-insulin resistance (HOMA-IR) ≥2.69 or <2.69, and by PCOS phenotype. Patients with PCOS-IR were treated with a 6-month course of cyproterone acetate/ethinyloestradiol with or without concomitant metformin. Measurements Inflammatory markers were examined at baseline, and after 6 months of treatment. Results A total of 445 women with PCOS (mean age 25.9 ± 2.7 years; 298 obese, 147 nonobese) and 213 normal controls (mean age 24.9 ± 3.0 years) were included. Regardless of obesity status, testosterone, free androgen index (FAI), luteinizing hormone/follicle-stimulating hormone (LH/FSH) ratio, HOMA-IR, TSP-1 and NF-κB in the PCOS groups were significantly higher than in the control group, whereas TSP-1 was lower in the PCOS groups (all, P < 0.05). Patients with PCOS without IR had lower TSP-1 levels than control patients (P < 0.05). Treatment with cyproterone acetate/ethinyloestradiol with addition of metformin reduced the level of NF-κβ, TGF-β1 and HOMA-IR and increased the level of TSP-1. Conclusions These results support the association between PCOS and chronic inflammation. [ABSTRACT FROM AUTHOR]