Abstract
Lung cancer and pulmonary tuberculosis caused by Mycobacterium are two major causes of deaths worldwide. Tuberculosis linked lung cancer is known. However, the precise molecular mechanism of Mycobacterium associated increased risk of lung cancer is not understood. We report 45 common human miRNAs deregulated in both pulmonary tuberculosis and lung cancer. We show that sRNA_1096 and sRNA_1414 from M. tuberculosis have sequence homology with human mir-21. Hence, the potential role of these three small non-coding RNAs in rifampicin resistance in pulmonary tuberculosis is implied. Further, the linking of sRNA_1096 and sRNA_1414 from M. tuberculosis with the host lung tumorigenesis is inferred. Nonetheless, further analysis and validation is required to associate these three non-coding RNAs with Mycobacterium associated increased risk of lung cancer.
Highlights
Viral involvements and their causal roles in oncology are well accepted for various cancers including ovarian neoplasms [1] hepatocellular carcinoma [2] and lung cancer [3] among others
We collected all the validated deregulated micro RNAs (miRNAs) associated with lung cancer and pulmonary tuberculosis from published literature indexed in PubMed and from databases such as miRegulome [32], miR2Disease [37], and TUMIR [38]
While we checked for the common miRNAs that are deregulated both in pulmonary tuberculosis and lung cancer, we found the number is only 45 (Supplementary Table S1, see supplementary data)
Summary
Viral involvements and their causal roles in oncology are well accepted for various cancers including ovarian neoplasms [1] hepatocellular carcinoma [2] and lung cancer [3] among others. Several reports have documented the co-existence of tuberculosis and lung cancer [14, 17,18,19,20], and pulmonary tuberculosis is a risk factor for developing lung cancer [17,18,19,20]. It is not yet fully established at the molecular level, how the Mycobacterium increases susceptibility to lung cancer. Some reports say that M. tuberculosis induces ROS mediated DNA damage pathway and produces epiregulin growth factor to induce cell proliferation [21]; while an other study indicates mechanisms along with COX-2 mediated activation of inflammatory pathway in M. tuberculosis associated carcinogenesis [22]
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