High expression of miR-155 and miR-21 in the recurrence or metastasis of non-small cell lung cancer

Abstract

High expression of miR-155 and miR-21 in the recurrence or metastasis of non-small cell lung cancer (NSCLC) was investigated. Retrospective analysis on the clinical information of 180 patients with NSCLC was carried out. The patients were admitted to Daqing Oil Field General Hospital from February 2012 to March 2015 and they were the research group. Moreover, the physical examination information of 88 normal medical examinees were selected at the same period of time as the control group. In the research group, 68 patients diagnosed with NSCLC were the newly diagnosed group and 112 cases of recurrence or metastasis of NSCLC were the recurrence group. The quantitative real-time polymerase chain reaction was used to detect the expression levels of serum miR-115 and miR-21. In addition, the expression levels between miR-155 and miR-21 and the relationship between the recurrence rate and metastasis of NSCLC were analyzed. The impact on the prognosis of patients were also analyzed. The expression levels of serum miR-155 and miR-21 were higher in the research group than those in the control group (P<0.05). The expression levels of serum miR-155 and miR-21 were higher in the recurrence group than those in the newly diagnosed group (P<0.05). We followed up the patients in the research group for 36 months, the median survival time and mortality rate in the recurrence group was higher than that of in the newly diagnosed group (χ 2 =9.705, P<0.01). In conclusion, miR-155 and miR-21 were highly expressed in the serum of patients, however, the recurrence and metastasis of NSCLC were even higher. The highly expressed levels of miR-155 and miR-21 were associated with the recurrence and metastasis in NSCLC patients, affecting the prognosis of patients.

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

“…In general, the deregulation of microRNA expression has been associated with gene alterations that are commonly linked to smoke-related cancers [67][68][69]. The "oncomirs" miR-21 and miR-155 have previously been associated with cancers of the upper aerodigestive tract [48,49,[51][52][53][54]. In particular, miR-21 has been considered as a marker of poor prognosis in lung and head and neck cancer [70,71].…”

“…Hypo-or hyper-methylation of miRNA was considered to represent a new level of complexity in gene regulation in human cancers [81], suggesting miR-21 or miR-155 promoter hypo-methylation [81][82][83][84] and miR-422a hyper-methylation, as previously reported for miR-373 [81,85], as potential epigenetic modifications caused by tobacco carcinogenic effects on MMR. On the other hand, alkylating agents, such as NNK can also directly or after biological activation react and form covalent bonds with nucleophilic centers found in DNA and RNA and proteins [86], supporting possible direct interference of NNK with levels of miRNAs, thereby causing their deregulation [48,49,[51][52][53][54]. Subsequently, NNK-induced miRNA deregulations can affect MMR gene expression, either thought post-transcriptional modifications or through DNA methylation by targeting DNA methyltransferases or methylation-related proteins [81].…”

“…Some reports have also shown that oncomir miR-21 downregulates hMSH2 gene expression by targeting the 3 untranslated region of its mRNA [45], and that miR-155 can significantly downregulate hMSH2, hMSH6, and hMLH1 [46], while others have suggested that miRNAs play an important role in modulating cell cycle progression by targeting hMSH2 in lung cancer [42]. Although there are reports suggesting a relationship between the MMR mechanism and miRNA profiles [41,43,44,46], the underlying molecular mechanism by which tobacco smoke carcinogens induce miRNA deregulation and affect the expression profiles of mismatch repair genes, particularly in lung and head and neck cancer, is not yet known.Here, we attempt to explore whether NNK affects the expression of small regulatory molecules, such as known miRNA markers, previously associated with upper aerodigestive tract malignancies [47][48][49][50][51][52][53][54] that may directly or indirectly be involved in the regulation for MMR expression phenotypes. Understanding the molecular changes induced by various risk factors, such as tobacco smoke, which promote the development and progression of cancer, will help to develop new diagnostic and therapeutic approaches [55,56], leading to optimization of their management.…”

“…Here, we attempt to explore whether NNK affects the expression of small regulatory molecules, such as known miRNA markers, previously associated with upper aerodigestive tract malignancies [47][48][49][50][51][52][53][54] that may directly or indirectly be involved in the regulation for MMR expression phenotypes. Understanding the molecular changes induced by various risk factors, such as tobacco smoke, which promote the development and progression of cancer, will help to develop new diagnostic and therapeutic approaches [55,56], leading to optimization of their management.…”

<p>circGFRA1 Enhances NSCLC Progression by Sponging miR-188-3p</p>

“…15 Xu et al reported that the expression of miR-155 and miR-21 was associated with the recurrence or metastasis of NSCLC. 16 MiR-188-3p has been reported to be a tumor suppressor in several cancers, including hepatocellular carcinoma, 17 breast cancer, 18 colorectal cancer, 19 and pancreatic cancer. 20 However, the function of miR-188-3p in NSCLC still remains unexplored.…”