Notably, all the studies conducted around the expression of miR-93 in lung cancer demonstrate that its upregulation is usually associated with poor prognosis of patients with lung cancer. cycle arrest by inhibition of miR-93 and consequently, stimulation of PTEN/Akt axis [298]. MiR-93 down-regulation is usually a potent biomarker of ovarian cancer with the sensitivity as much as 93% [299]. Colorectal cancer Colorectal cancer (CRC) is considered as the third leading cause of death [300]. This life threatening disorder has high metastasis capability and there have been attempts to evaluate the molecular signaling pathways involved in its progression [301, 302]. It is held that lncRNA CA3-AS1 is usually capable of reducing the malignancy of colorectal cancer cells by inhibition of miR-93 and consequently, induction of PTEN as a tumor suppressor [303]. MiR-93 Bleomycin hydrochloride and angiogenesis Angiogenesis is one of the most important mechanisms involved in delivering oxygen and nutrients to the tumor cells [304]. It seems that this mechanism plays a remarkable role in a variety of stages of cancer such as proliferation and migration [305]. Anti-angiogenic brokers have exhibited great potential in inhibition of malignancy and invasion of cancer cells [306, 307]. There are two major problems associated with inhibition of angiogenesis: A) it appears that the introduced anti-angiogenic drugs are capable of suppressing angiogenesis in a just a number of cancers, and B) some of the tumor cells are able to advance without angiogenesis enhancing the complexity of cancer [308]. So, elucidating the molecular pathways involved in angiogenesis is suggested to be beneficial in cancer therapy. Upregulation of miR-93-5p increases the angiogenesis capability of human umbilical vein endothelial cells (HUVECs) Bleomycin hydrochloride leading to the improvement in blood vessel density, high proliferation and migration, and enhanced lumen formation and sprouting [309]. The interesting point of this study is the role of molecular signaling pathways. Epithelial protein lost in neoplasm (EPLIN) is usually a cytoskeleton-associated protein that plays a significant role in supervising the cell motility and actin dynamics. It has been exhibited that high expression of EPLIN is related to the reduced ability of HUVECs in migration and tubule formation [310]. As a consequence, based on the efficiency of miR-93-5p in enhancing the angiogenesis and cell motility of HUVECs, it seems that this miR exerts Rabbit polyclonal to SZT2 inhibitory impact on EPLIN [309]. Conclusion and remarks This review provided a comprehensive discussion about the role of miR-93 in various malignancy cell lines. Notably, all the studies conducted around the Bleomycin hydrochloride expression of miR-93 in lung cancer demonstrate that its upregulation is usually associated with poor prognosis of patients with lung cancer. More importantly, these studies imply that miR-93 is an oncogenesis miR in lung cancer that favors conditions into high proliferation and viability of lung cancer cells. The same story occurs in EC cancer. This miR not only serves as a biomarker during EC generation but also enhances the malignancy of cancer cells by inhibition of PTEN/PI3K/Akt signaling pathway. MiR-93/FZD7/Wnt axis is also important for promoting the progression of OS cells. It is noteworthy that this studies involving in the role of miR-93 in EC, OS and cervical cancers are low in number and more studies are required to clarify the oncogenesis or oncosuppressor impact of miR-93. But these experiments highlight the oncogenesis impact of miR-93. Interestingly, accumulating data demonstrates that miR-93 indirectly stimulates PI3K/Akt pathway to elevate the proliferation and malignancy of brain tumors. In this way, miR-93 suppresses the expression of PTEN, PHLPP, and FOXO3. It seems that miR-93 affects much more molecular pathways in prostate cancer. Figure?1 obviously shows these pathways. LncRNAs play a significant role in suppressing HCC. LncRNAs SNHG16 and LINC00472 exert inhibitory impact on the progression of HCC cells by.