Long non-coding RNAs (lncRNAs) exhibit a length more than 200 nucleotides and they are characterized by non-coding RNAs (ncRNA) not encoded into proteins. Over the past few years, the role and development of lncRNAs have aroused the rising attention of researchers. To be specific, KCNQ1OT1, the KCNQ1 opposite strand/antisense transcript 1, is clearly classified as a regulatory ncRNA. KCNQ1OT1 is capable of interacting with miRNAs, RNAs and proteins, thereby affecting gene expression and various cell functions (e.g., cell proliferation, migration, epithelial–mesenchymal transition (EMT), apoptosis, viability, autophagy and inflammation). KCNQ1OT1 is dysregulated in a wide range of human diseases (e.g., cardiovascular disease, cancer, diabetes, osteoarthritis, osteoporosis and cataract), and it is speculated to act as a therapeutic target for treating various human diseases. On the whole, this review aims to explore the biological functions, underlying mechanisms and pathogenic roles of KCNQ1OT1 in human diseases.

The frequency of human suffering from cancer is increasing annually across the globe. This has fueled numerous investigations aimed at the prevention and cure of various cancers. Long non-coding RNA (lncRNA) are known to play a crucial role in cancer. For instance, cancer susceptibility candidate 11 (CASC11), as one of the long non-coding RNAs, has been reported to be overexpressed in various tumors. This review elucidates the mechanism by which lncRNA CASC11 regulates tumors' biological processes and affirms its value as a therapeutic target for tumors. Through systematic analysis and review of relevant articles in PubMed, we revealed the pathophysiological mechanism of CASC11 on the tumor by regulating the biological processes of tumor such as proliferation, autophagy, apoptosis, thereby promoting tumor metastasis. We also revealed the regulatory pathways of CASC11 in different tumors, for instance by acting on a variety of microRNAs, oncogenic proteins, carcinogens, and transcription factors. Consequently, CASC11 regulates cancer proliferation, apoptosis, and invasion by altering the WNT/β-catenin signaling pathway and epithelial–mesenchymal transition (EMT). Furthermore, CASC11 expression has a high pertinence with clinical prognosis, suggesting that it is a potential marker for malignant tumors or a clinical adjuvant therapy in the future.

Among the gynecological cancers, ovarian cancer is the most lethal. Its therapeutic options include a combination of chemotherapy with platinum-based compounds and cytoreductive surgery. Most ovarian cancer patients exhibit an initial response to platinum-based therapy, however, platinum resistance has led to up to 80% of this responsive cohort becoming refractory. Ovarian cancer recurrence and drug resistance to current chemotherapeutic options is a global challenge. Chemo-resistance is a complex phenomenon that involves multiple genes and signal transduction pathways. Therefore, it is important to elucidate on the underlying molecular mechanisms involved in chemo-resistance. This inform decisions regarding therapeutic management and help in the identification of novel and effective drug targets. Studies have documented the individual biomarkers of platinum-resistance in ovarian cancer that are potential therapeutic targets. This review summarizes the molecular mechanisms of platinum resistance in ovarian cancer, novel drug targets, and clinical outcomes.

Astragalus and Angelica decoction (A&A) has been clinically used as a classical traditional Chinese medicine (TCM) formula in China for many years for the treatment of kidney diseases, especially renal interstitial fibrosis (RIF). However, the mechanisms underlying the therapeutic effects of A&A on RIF remains poorly understood. In the present study, systematic network pharmacology and effective experimental verification were utilized for the first time to elucidate the pharmacological efficacy and potential mechanism. The outcomes indicated that 22 active components and 87 target genes of A&A were identified and cross-referenced with RIF-associated genes, contributing to confirmation of 74 target genes of A&A for RIF. Pathway and functional enrichment analyses revealed that A&A had substantial effects on MAPK, PI3K-Akt and TNF signaling pathways. In addition, seven core targets with relatively higher betweenness and degree were identified in the constructed Chinese medicine material-chemical component-target-signal pathway network. Moreover, we verified the potential therapeutic effect of A&A in vivo (using a mouse model of RIF), confirming that A&A could effectively protect the kidney by regulating these target genes. The therapeutic effect of A&A on RIF could be attributed to its role in regulating the cell cycle, limiting the apoptosis, and inhibiting the inflammation.

Traumatic brain injury (TBI) is the major cause of high mortality and disability rates worldwide. Pioglitazone is an activator of peroxisome proliferator-activated receptor-gamma (PPARγ) that can reduce inflammation following TBI. Clinically, neuroinflammation after TBI lacks effective treatment. Although there are many studies on PPARγ in TBI animals, only few could be converted into clinical, since TBI mechanisms in humans and animals are not completely consistent. The present study, provided a potential theoretical basis and therapeutic target for neuroinflammation treatment after TBI. First, we detected interleukin-6 (IL-6), nitric oxide (NO) and Caspase-3 in TBI clinical specimens, confirming a presence of a high expression of inflammatory factors. Western blot (WB), quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) were used to detect PPARγ, IL-6, and p-NF-κB to identify the mechanisms of neuroinflammation. Then, in the rat TBI model, neurobehavioral and cerebral edema levels were investigated after intervention with pioglitazone (PPARγ activator) or T0070907 (PPARγ inhibitor), and PPARγ, IL-6 and p-NF-κB were detected again by qRT-PCR, WB and immunofluorescence (IF). The obtained results revealed that: 1) increased expression of IL-6, NO and Caspase-3 in serum and cerebrospinal fluid in patients after TBI, and decreased PPARγ in brain tissue; 2) pioglitazone could improve neurobehavioral and reduce brain edema in rats after TBI; 3) the protective effect of pioglitazone was achieved by activating PPARγ and reducing NF-κB and IL-6. The neuroprotective effect of pioglitazone on TBI was mediated through the PPARγ/NF-κB/IL-6 pathway.