MALAT1: A key regulator in lung cancer pathogenesis and therapeutic targeting.

Lung cancer remains a formidable global health burden, necessitating a comprehensive understanding of the underlying molecular mechanisms driving its progression. Recently, lncRNAs have become necessary controllers of various biological functions, including cancer development. MALAT1 has garnered significant attention due to its multifaceted role in lung cancer progression. Lung cancer, among other malignancies, upregulates MALAT1. Its overexpression has been associated with aggressive tumor behavior and poor patient prognosis. MALAT1 promotes cellular proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis in lung cancer, collectively facilitating tumor growth and metastasis. Additionally, MALAT1 enhances cancer cell invasion by interacting with numerous signaling pathways. Furthermore, MALAT1 has been implicated in mediating drug resistance in lung cancer, contributing to the limited efficacy of conventional therapies. Recent advancements in molecular biology and high-throughput sequencing technologies have offered fresh perspectives into the regulatory networks of MALAT1 in lung cancer. It exerts its oncogenic effects by acting as a ceRNA to sponge microRNAs, thereby relieving their inhibitory effects on target genes. Moreover, MALAT1 also influences chromatin remodeling and post-translational modifications to modulate gene expression, further expanding its regulatory capabilities. This review sheds light on the multifaceted roles of MALAT1 in lung cancer progression, underscoring its potential as an innovative therapeutic target and diagnostic biomarker. Targeting MALAT1 alone or combined with existing therapies holds promise to mitigate lung cancer progression and improve patient outcomes.

Retraction of "Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis".

[This retracts the article DOI: 10.1021/acsomega.9b04357.].

Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis.

Multiple effects on cancer cells are exerted by the peroxisome proliferator-activated receptor γ (PPAR-γ). Recent studies have shown that rosiglitazone, a synthetic PPAR-γ ligand, inhibits the growth of cells. This research was designed to assess the impact of rosiglitazone on diethylnitrosamine (DENA)-induced lung carcinogenesis in Wistar rats and to study the underlying molecular mechanism. A total of 40 adult male Wistar rats were separated into four groups as follows: group 1 is known as a control. Group 2 is known as the DENA group (150 mg/kg, i.p.). Group 3 and group 4 denote DENA-induced rats treated with 5 and 10 mg/kg rosiglitazone, respectively. Lipid peroxidation, various antioxidant enzymes, histological perceptions, and caspase-3, Bcl2, and Bax gene expression were measured in lung tissues. Rosiglitazone treatment reverted the DENA-induced changes in the expression of these genes, inflammatory cytokines, and oxidative stress. However, blotting analysis discovered reduced caspase-3 and BAX expressions and elevated Bcl-2 expression in DENA-induced rats. The expression of such proteins causing DENA lung cancer was restored by rosiglitazone therapy.

Metformin: A Salutary Candidate for Colorectal Cancer Treatment in Patients with Diabetes.

The current study is a review of the literature on patients with diabetes who are diagnosed with colorectal cancer (CRC), encompassing recent research on CRC and the molecular level changes occurring in these patients on the basis of varying environmental as well as non-environmental factors. It has been noted that nearly 50% of all patients undergo the systemic treatment module; however, most of them exhibit drug resistance. In addition, targeted gene therapy has also been used in treatment but has been found to be effective only in patients with a specified molecular profile (or else this might lead to an increased risk of developing resistant mutations). This has led to increasing interest among researchers in finding innovative treatment options. Metformin, a biguanide, has been widely used in treating diabetes. The drug has been reportedly used in cases of hypothesis-generating retrospective population studies of diabetic patients showing reduced incidence of cancer. Metformin helps in reduction of excess insulin levels that possess various effects on cell signaling and metabolism. Nonetheless, there is need for an in-depth study on its molecular mechanism to fill any existing research gaps.

Combinational effect of angiotensin receptor blocker and folic acid therapy on uric acid and creatinine level in hyperhomocysteinemia-associated hypertension.

Homocysteine [HSCH2 CH2 CH(NH2 )COOH] (Hcy) is a sulfur-containing amino acid of 135.18 Da of molecular weight, generated during conversion of methionine to cysteine. If there is a higher accumulation of Hcy in the blood, that is usually above 15 µmol/L, it leads to a condition referred to as hyperhomocysteinemia. A meta-analysis of observational study suggested an elevated concentration of Hcy in blood, which is termed as the risk factors leading to ischemic heart disease and stroke. Further experimental studies stated that Hcy can lead to an increase in the proliferation of vascular smooth muscle cells and functional impairment of endothelial cells. The analyses confirmed some of the predictors for Hcy presence, such as serum uric acid (UA), systolic blood pressure, and hematocrit. However, angiotensin-converting enzyme inhibitors angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) alone are inadequate for controlling UA and creatinine level, although the addition of folic acid may be beneficial in hypertensive patients who are known to have a high prevalence of elevated Hcy. We hypothesized that combination therapy with an ARB (olmesartan) and folic acid is a promising treatment for lowering the UA and creatinine level in hyperhomocysteinemia-associated hypertension.