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Anaplastic thyroid cancer (ATC) remains as one of the most aggressive human carcinomas with poor survival rates in patients with the cancer despite therapeutic interventions. Novel targeted and personalized therapies could solve the puzzle of poor survival rates of patients with ATC. In this review, we discuss the role of non-coding RNAs in the regulation of gene expression in ATC as well as how the changes in their expression could potentially reshape the characteristics of ATCs. A broad range of miRNA, such as miR-205, miR-19a, miR-17-3p and miR-17-5p, miR-618, miR-20a, miR-155, etc., have abnormal expressions in ATC tissues and cells when compared to those of non-neoplastic thyroid tissues and cells. Moreover, lncRNAs, such as H19, Human leukocyte antigen (HLA) complex P5 (HCP5), Urothelial carcinoma-associated 1 (UCA1), Nuclear paraspeckle assembly transcript 1 (NEAT1), etc., participate in transcription and post-transcriptional regulation of gene expression in ATC cells. Dysregulations of these non-coding RNAs were associated with development and progression of ATC by modulating the functions of oncogenes during tumour progression. Thus, restoration of the abnormal expression of these miRNAs and lncRNAs may serve as promising ways to treat the patients with ATC. In addition, siRNA mediated inhibition of several oncogenes may act as a potential option against ATC. Thus, non-coding RNAs can be useful as prognostic biomarkers and potential therapeutic targets for the better management of patients with ATC.

Background: Syzygium cumini, one of the evidence-based traditional medicinal plant used in the treatment of various ailments. Objectives: Herein, the antioxidant property and anticancer property of Syzygium cumini against Ehrlich Ascites Carcinoma (EAC) were examined in search of effective chemotherapeutics. Methods: In vitro assays, phytochemical and chromatographic analysis were used to determine antioxidant properties and chemical constituents of Syzygium cummini bark methanolic extract (SCBME). Functional assays were used to measure the anticancer activity of SCBME. Fluorescence microscopy and RT-PCR were used to examine morphological and molecular changes of EAC cells followed by SCBME treatment. Results: Phytochemical and GC–MS analysis confirmed the presence of compounds with antioxidant and anticancer activities. Accordingly, we have noted a strong antioxidant activity of SCBME with an IC50 value of 10μg/ml. Importantly, SCBME exerted a dose-dependent anticancer activity with significant inhibition of EAC cell growth (71.08 ± 3.53%; p<0.001), reduction of tumour burden (69.50%; p<0.01) and increase of life span (73.13%; p<0.001) of EACbearing mice at 75mg/kg/day. Besides, SCBME restored the blood toxicity towards normal in EAC-bearing mice (p<0.05). SCBME treated EAC cells showed apoptotic features under a fluorescence microscope and fragment DNA in DNA laddering assay. Moreover, up-regulation of the tumour suppressor p53 and pro-apoptotic Bax and down-regulation of NF-κB and anti-apoptotic Bcl-2 genes, implied induction of apoptosis followed by SCBME treatment. Conclusion: The antiproliferative activity of SCBME against EAC cells is likely due to apoptosis, mediated by regulation of p53 and NF-κB signalling. Thus, SCBME can be considered as a useful resource in cancer chemotherapy.

Angiotensin Converting Enzyme (ACE) regulates blood pressure. ACE converts angiotensin I to angiotensin II which binds with its receptors and through a cascade of reactions constrict blood vesels, consequently results in increased blood pressure, called hypertension. Inhibition of ACE activity is considered as an useful therapeutic target that reduce hypertension. Moringa oleifera leaves have traditionally been used in Ayurvedic medicine for their antihypertensive activity and antihypertensive effect of Moringa leaves was reported on spontaneously hypertensive rats. So, we hypothesize that Moringa oleifera leaves methanolic extract (MOLME) might inhibit ACE activity. Inhibition of ACE activity by MOLME was estimated in vitro. In this study, inhibition of ACE by MOLME was evaluated by spectrophotometric method. MOLME inhibited ACE activity in the substrate hippuryl-Lhistidyl-L-leucine (HHL) with an IC50 value of 226.37 μg/ml with a reference compound, captropril (CP), a potent ACE inhibitor with an IC50 value of 0.0289 μM. The mode of ACE inhibition in HHL with or without MOLME revealed that the Vmax (0.0857 and 0.0541 OD/30 min, respectively) was changed and the Km values were 4.671 and 4.41. The results indicate that MOLME acts as a non-competitive inhibitor for ACE. CP was found a competitive inhibitor of ACE. MOLME might be a potential natural inhibitor of ACE which reduces hypertension.

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