## 4 Discussion
Furthermore, we could mention the great diversity of siRNA targets that were developed among these studies. They focused on a wide variety of possible pathways and expressions within the tumor cell, which in many cases are under-regulated or in an aberrant state. For example, we can mention the targeting of overexpression of Bcl-2, a protein that helps control the survival or destruction of a tumor cell by preventing apoptosis and the family of which is regulated through post-translational modifications and interactions with other proteins, allowing them to serve as crucial nodal points at the intersection of multiple pathways with significant relevance to oncology [40]. These proteins regulate all major forms of cell death, including apoptosis, necrosis, and autophagy, and can modulate various cell death mechanisms. This elevated expression is observed in nearly half of all human cancers and usually results in the loss of the tumor suppressor function of these killer genes, thereby inhibiting cell death, including that induced by cytotoxic anticancer drugs. For this reason, it has become an interesting target for different strategies to induce tumoral cell death [70]. Regarding the inhibited molecular pathways, we found targets located in the same signaling pathways, in different but correlated pathways due to their cellular effects, or even targets located in independent pathways or specific protein expressions. For example, within this last subdivision, we can find COL1A1, a cancer-promoting factor whose accumulation is correlated with dysregulation of the epithelial-mesenchymal transition and tumorigenesis [29]; IDO-1, which is integrating the kynureine pathway related to tumor neovascularization through modulating the expression of interferon-gamma (IFN-\(\gamma\)) and tumor immunosuppression [26]; LDHA, related to the growth and proliferation of tumor cells through the secretion of lactic acid and the activation of the epithelial-mesenchymal transition [25]; UBR, associated with the Arg/N-degorn pathway, related to cell cycle control [43]; VEGF, present in its own signaling pathway for stimulating angiogenesis; PLK1, linked to the regulation of the G2/M transition and the initiation of cancer through activation of CDC25 via the PLK signaling pathway cascade, among others [59]. However, we can also exemplify cases of different siRNA targets that have an influence on the same signaling pathway. For example, si-SHP-1 [52], which influences as a multi-regulator of signals in the JAK/STAT3 signaling pathway, as well as si-Bmi-1, is involved in most signaling pathways, including JAK/STAT3, and present in the DDR pathway of ROS reduction [51]. In addition, C-Met and HGF were both associated with the activation of key oncogenic pathways such as STAT3, PI3K, or RAS, and with processes of organogenesis and metastasis. Furthermore, regarding the PI3K pathway, targets such as PD-L1 are also notable, related to immune system suppression and tumor proliferation, and associated with it, ATP7A was positively related to tumor infiltration and the detoxification of copper in tumor cells, preventing apoptosis [22]. Also, within the PI3K/AKT pathway, we can find the target PCBP2, essential in the apoptotic pathway and present in the STAT3 pathway. Finally, EpCAM was also associated with the regulation of this pathway, being linked to increased cellular proliferation and differentiation, angiogenesis, and metastasis [47; 57]. In addition, HER2, related to the control of cell division and the survival of tumor cells, was also present in the mTOR pathway [35; 40; 44; 60; 62; 63; 68]. Noteworthy also is the Bcl-2 pathway, comprised of Bcl-2 itself, linked to the regulation of the induction of apoptosis; Mcl-1, anti-apoptotic; and MK, related to the proliferation of cancer cells and the activation of Bcl-2, also associated with the mTOR and VEGF-A pathways.