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HIV-infected people are also at an increased risk of \u201cnon-AIDS-defining\u201d malignancies not directly linked to immune suppression but associated with viral infections. Their incidence is increasing despite successful antiretroviral therapy. The mechanism behind this phenomenon remains unclear. Here, we obtained daughter clones of murine mammary gland adenocarcinoma 4T1luc2 cells expressing consensus reverse transcriptase of HIV-1 subtype A FSU_A strain (RT_A) with and without primary mutations of drug resistance. In<jats:italic>in vitro<\/jats:italic>tests, mutations of resistance to nucleoside inhibitors K65R\/M184V reduced the polymerase, and to nonnucleoside inhibitors K103N\/G190S, the RNase H activities of RT_A. Expression of these RT_A variants in 4T1luc2 cells led to increased production of the reactive oxygen species (ROS), lipid peroxidation, enhanced cell motility in the wound healing assay, and upregulation of expression of<jats:italic>Vimentin<\/jats:italic>and<jats:italic>Twist<\/jats:italic>. These properties, particularly, the expression of<jats:italic>Twist<\/jats:italic>, correlated with the levels of expression RT_A and\/or the production of ROS. When implanted into syngeneic BALB\/C mice, 4T1luc2 cells expressing nonmutated RT_A demonstrated enhanced rate of tumor growth and increased metastatic activity, dependent on the level of expression of RT_A and<jats:italic>Twist<\/jats:italic>. No enhancement was observed for the clones expressing mutated RT_A variants. Plausible mechanisms are discussed involving differential interactions of mutated and nonmutated RTs with its cellular partners involved in the regulation of ROS. This study establishes links between the expression of HIV-1 RT, production of ROS, induction of EMT, and enhanced propagation of RT-expressing tumor cells. Such scenario can be proposed as one of the mechanisms of HIV-induced\/enhanced carcinogenesis not associated with immune suppression.<\/jats:p>","DOI":"10.1155\/2019\/6016278","type":"journal-article","created":{"date-parts":[[2019,12,2]],"date-time":"2019-12-02T23:34:57Z","timestamp":1575329697000},"page":"1-28","source":"Crossref","is-referenced-by-count":27,"title":["HIV-1 Reverse Transcriptase Promotes Tumor Growth and Metastasis Formation via ROS-Dependent Upregulation of Twist"],"prefix":"10.1155","volume":"2019","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6160-2203","authenticated-orcid":true,"given":"Ekaterina","family":"Bayurova","sequence":"first","affiliation":[{"name":"NF Gamaleya Research Center of Epidemiology and Microbiology, Moscow, Russia"},{"name":"Chumakov Federal Scientific Center for Research and Development of Immune-and-Biological Products of Russian Academy of Sciences, Moscow, 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