Current Molecular Medicine - Current Issue

The plague caused by Yersinia pestis has a high case fatality rate. It is often transmitted from person to person through mosquito bites, causing serious disease transmission. Due to its clinical symptoms being very similar to influenza, it is difficult to detect by people. Traditional detection methods for Y. pestis mainly include bacterial culture and serological identification, which are cumbersome and require high experimental conditions. Therefore, a fast and effective detection method is very important. At present, polymerase chain reaction (PCR) is one of the methods for rapid detection of Y. pestis. In this review, we focus on the application, advantages, and disadvantages of multiplex PCR technology in clinical detection.

Neuropathological diseases involve the death of neurons and the aggregation of proteins with altered properties in the brain. Proteins are used at the molecular level to categorize neurodegenerative disorders, emphasizing the importance of protein-processing mechanisms in their development. Natural herbal phytoconstituents, such as icariin, have addressed these neurological complications. Icariin, the principal compound in Epimedium, has been studied for its anti-neuroinflammatory, anti-oxidative, and antiapoptotic properties. Recent scientific investigations have shown that icariin exhibits promising therapeutic and preventive properties for mental and neurodegenerative disorders. In preclinical, icariin has been shown to inhibit amyloid development and reduce the expression of APP and BACE-1. Previous preclinical studies have demonstrated that icariin can regulate proinflammatory responses in neurological conditions like Parkinson's disease, depression, cerebral ischemia, ALS, and multiple sclerosis. Studies have shown that icariin possesses neuroprotective properties by modulating signaling pathways and crossing the blood-brain barrier, suggesting its potential to address various neurocomplications. This review aims to establish a foundation for future clinical investigations by examining the existing literature on icariin and exploring its potential therapeutic implications in treating neurodegenerative disorders and neuropsychiatric conditions. Future research may address numerous concerns and yield captivating findings with far-reaching implications for various aspects of icariin.

Oxidative stress is a consequence of the disruption of the balance between the generation of reactive nitrogen and oxygen species and the biological system’s ability to neutralize those reactive products. Oxidative stress is involved in the generation of many disorders, including epilepsy, which is a prevalent chronic neurological disease that affects the lives of millions of people around the world. Epilepsy is characterized by unforeseeable and repeated seizures that can be very disturbing. Studies have reported that oxidative stress occurs before and after seizures. A transcription factor named Nuclear factor erythroid-derived 2-related factor 2 (Nrf2) controls genes related to the induction of oxidative stress and defends cells against oxidative stress. The Nrf2 protein has seven different domains, ranging from Neh1 to Neh7. Each domain is responsible for a distinctive function of this protein. Keap1 binds to Nrf2, but during oxidative stress, Nrf2 detaches from the Keap1 protein, moves to the nucleus, and binds to DNA. The result of this translocation and binding is the initiation of transcription of detoxifying genes to control the harmful effects of oxidative stress. There is some evidence of oxidative stress involvement in epilepsy. In this review, we have listed potential Nrf2-related therapeutic targets for treating and controlling epilepsy, such as Berberis alkaloids, pentoxifylline, lovastatin, progesterone, and chrysin nanoparticles. These activators were tested in animals (in vivo) and cells (in vitro), and most of these experiments showed promising results in different epilepsy models. Finally, the results have suggested that the activation of Nrf2 can be an option for controlling epilepsy.

Vitamin C plays a significant role in various physiological functions. Humans depend on external sources of vitamin C due to the loss of the L-gulono-γ-lactone oxidase (GULO) gene that contributes to the synthesis of vitamin C. During the evolutionary loss of the GULO gene, physical, chemical, and biological factors were different from the present environmental settings. Besides the evolutionary genetic loss of the GULO gene, there is a gap in the insightful discussion on the potential implications of the non-functional GULO gene towards the predisposition of humans to cancer that faces hostile and carcinogenic environments. Various methods by which vitamin C modulates cellular processes related to cancer, including DNA repair, epigenetic changes, and redox balance, are discussed. Furthermore, we present experimental and clinical evidence indicating that vitamin C deficiency promotes tumor growth, metastasis, and therapy resistance, emphasizing its potential as a cancer phenotypic modulator. Therapeutic implications of restoring vitamin C levels in cancer treatment range from improving the efficacy of conventional medicines to exploiting metabolic vulnerabilities in tumors. The relevance of assessing vitamin C status in cancer patients and the basis for additional research into vitamin C supplementation as an adjuvant therapy is emphasized. This paper presents a comprehensive overview of the implications associated with the functional deficiency of the GULO gene in human subjects exhibiting diverse tumor hallmarks, encompassing ECM remodeling, hypoxia, epigenetic reprogramming, oxidative stress, and drug responsiveness.

Thyroid cancer is the most prevalent form of endocrine cancer. Therefore, the administration of new therapeutic agents for thyroid cancer patients is necessary. One of the recent successes in thyroid cancer research is the identification of the role of signaling pathways in the pathogenesis of the disease. Emerging evidence reveals that long non-coding RNAs (lncRNAs) can serve as novel therapeutic approaches for the diagnosis and treatment of thyroid cancer. The lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) plays key roles in gene expression, RNA processing, and epigenetic regulation. It is believed that MALAT1 can regulate several cancer-related processes, including tumour cell growth, proliferation, and metastasis. MALAT1 is involved in the pathogenesis of thzroid cancers by targeting multiple downstream targets and miRNA/mRNA axes. Here, we summarize the emerging roles of MALAT1 in this cancer.

Long non-coding RNAs (lncRNAs) refer to a group of RNA molecules that exceed a length of 200 nucleotides and lack the ability to code proteins. Numerous studies suggest that lncRNAs significantly contribute to the onset and progression of various forms of cancers. A specific lncRNA, known as long non-coding RNA 01296 (LINC01296), is extensively expressed in human malignancies. The level of LINC01296 has been shown to correlate with the progression and prognosis of cancers. Moreover, numerous scientific investigations have provided evidence that the dysregulation of LINC01296 functioning as a competitive endogenous RNA (ceRNA) exerts a profound influence on various aspects of cancer cell behavior, including proliferation, apoptosis, invasion, metastasis, and cell cycle progression, by means of regulating target genes and signaling pathways. An increasing body of data strongly suggests that LINC01296 may serve as a valuable biomarker for predicting cancer prognosis and could represent a promising therapeutic target for cancer intervention. In this comprehensive review, we summarize the recent advancements in our understanding of the role, underlying mechanisms, and clinical significance of LINC01296 in malignant tumors. The findings suggest that LINC01296 may be both a reliable biomarker and a potential therapeutic target for cancers.