Oncogene addiction to oncomiRs has been proposed in several human cancers [19, 40, 41]. A lot of studied showed that the aberrant expression miRNAs, including miR-21, miR-221/222, miR-181s and miR-34s, played an important role in gliomagenesis [42–45]. Overexpression of miR-21 could lead to a malignant phenotype, demonstrating that mir-21 was a genuine oncogene. When miR-21 was inactivated, the tumours regressed completely in a few

days, partly as a result of apoptosis [42]. And miR-181a and 181b functioned as tumor suppressors in glioma cells [44]. These results demonstrate that tumors could become addicted www.selleckchem.com/products/c646.html to oncomiRs and support efforts in treating human cancers through pharmacological inactivation of miRNAs such as miR-21 or upregulation

of miR-181s. Clinical implications of oncogene addiction in molecular targeted therapy for gliomas Chemotherapeutic agent therapy or molecular targeted therapy always works in tumors with certain respective genetic background. A growing body of genetic aberrations was identified in gliomas, only a subset of Cyclopamine supplier genes acting as drivers in carcinogenesis can be recognized as oncogene addition. Meanwhile, most genes just act as downstream effectors of addicted oncogenes. Oncogene addiction is an ideal potential target for molecular targeted therapy in human cancers. Therapies targeting genes causally linked to carcinogenesis have been successful in a subset of tumor types [46]. Each subtype of gliomas may display a different oncogene addiction. Some molecular targeted drugs only work in a subgroup of tumor patients. The choice of the appropriate molecular targeted

IMP dehydrogenase agent and combination therapy for a specific patient with cancer is largely empirical. In theory, it is essential to define specific oncogene addiction for individuals before choosing molecular targeted drugs. It should be pointed out that distinct kinds of cells in one sample (e.g. CD133- and CD133+ cells) have different oncogene addictions due to the heterogeneity of glioma. Thus combination of multiple drugs is required to target more than one oncogene addictions in one patient. In addition, oncogene addiction is always moving as the therapeutic targets in gliomas. After exposure to therapeutic agents, cancer cells can escape from one established oncogene addition to another. At this situation, previous drugs would not work anymore. This may be the reason of acquired drug resistance. We named the above phenomenon to “”Oncogene addiction transition”". Studies are needed for further investigating possible direction of oncogene addiction transition, which is important for choosing rational scheme of combination therapy.