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1.
Int J Mol Sci ; 25(3)2024 Jan 26.
Article in English | MEDLINE | ID: mdl-38338839

ABSTRACT

Autophagy, a complex and highly regulated cellular process, is critical for the maintenance of cellular homeostasis by lysosomal degradation of cellular debris, intracellular pathogens, and dysfunctional organelles. It has become an interesting and attractive topic in cancer because of its dual role as a tumor suppressor and cell survival mechanism. As a highly conserved pathway, autophagy is strictly regulated by diverse non-coding RNAs (ncRNAs), ranging from short and flexible miRNAs to lncRNAs and even circRNAs, which largely contribute to autophagy regulatory networks via complex RNA interactions. The potential roles of RNA interactions during autophagy, especially in cancer procession and further anticancer treatment, will aid our understanding of related RNAs in autophagy in tumorigenesis and cancer treatment. Herein, we mainly summarized autophagy-related mRNAs and ncRNAs, also providing RNA-RNA interactions and their potential roles in cancer prognosis, which may deepen our understanding of the relationships between various RNAs during autophagy and provide new insights into autophagy-related therapeutic strategies in personalized medicine.


Subject(s)
MicroRNAs , Neoplasms , RNA, Long Noncoding , Humans , RNA, Untranslated/genetics , MicroRNAs/genetics , MicroRNAs/metabolism , Neoplasms/genetics , RNA, Messenger/genetics , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Autophagy/genetics
2.
Minerva Endocrinol ; 44(3): 259-263, 2019 Sep.
Article in English | MEDLINE | ID: mdl-29205013

ABSTRACT

BACKGROUND: This paper aimed to investigate the regulating role of adipokine expression level in body fat distribution of patients with type 2 diabetes mellitus (T2MD) as well as its correlation with metabolic syndrome (MS). METHODS: One hundred forty patients with T2MD admitted in the Endocrinology Department of the First Affiliated Hospital of Liaoning University of Traditional Chinese Medicine from January 2017 to July 2017 were selected; their body height and weight were measured to calculate Body Mass Index (BMI); patients with a BMI ≤23.9 kg/m2 were included into control group (N.=49), and those with a BMI ≥24 kg/m2 into observation group (N.=91). Based on whether the patients were complicated with MS, they were divided into non-metabolic syndrome (N-MS) group (N.=79) and MS group (N.=61); the levels of serum dipeptidyl peptidase-4 (DPP-4), adiponectin (ADPN) and leptin as well as the contents of body fat and lean tissue of the two groups of patients were measured. RESULTS: The serum DPP-4 level in observation group was remarkably elevated compared with that in control group (P<0.05), but there were no significant differences in the leptin and ADPN levels between the two groups (P>0.05). The serum DPP-4 and leptin levels were positively correlated with the total body fat mass (FAT) of the patients in observation group (r=0.461, P=0.004; r=0.433, P=0.007); DPP-4 level had a positive correlation with trunk fat mass (TRUNK F) (r=0.545, P=0.001) and limb fat mass (LIMB F) (r=0.412, P=0.005); the leptin level was positively correlated with LIMB F (r=0.513, P=0.001); the leptin and ADPN levels were negatively correlated with the content of lean tissue (r=-0.476, P=0.001; r=-0.344, P=0.021). Compared with those in N-MS group, the levels of serum DPP-4 and leptin were increased significantly, while the ADPN level was decreased notably (P<0.05) in MS group. CONCLUSIONS: The adipokines DPP-4 and leptin in the serum can influence the body fat distribution of patients with T2MD; there is an important association of DPP-4, leptin and ADPN levels with MS, which may be used as therapeutic targets for multiple metabolism disorders of T2MD.


Subject(s)
Adipokines/blood , Body Fat Distribution , Diabetes Mellitus, Type 2/complications , Metabolic Syndrome/blood , Absorptiometry, Photon , Adiponectin/blood , Adult , Body Mass Index , Dipeptidyl Peptidase 4/blood , Female , Humans , Leptin/blood , Male , Metabolic Syndrome/etiology , Middle Aged
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