Abstract
Long non-coding RNAs (ncRNAs), which do not encode proteins, regulate cell proliferation, tumor angiogenesis, and metastasis and are closely associated with the development, progression, and metastasis of many cancers. Tumor-associated macrophages (TAMs) in the tumor microenvironment play an important role in cancer progression. The Hippo signaling pathway regulates cell proliferation and apoptosis, maintains tissue and organ size, and homeostasis of the internal environment of organisms. Abnormal expression of Yes-associated protein (YAP), the Hippo signaling pathway key component, is widely observed in various malignancies. Further, TAM, lncRNA, and YAP are currently valuable targets for cancer immunotherapy. In this review, we have logically summarized recent studies, clarified the close association between the three factors and tumorigenesis, and analyzed the outlook of tumor immunotherapy.
Highlights
The human genome, which typically encodes both coding and non-coding transcripts, contains a large amount of apparently functional but non-coding DNA that is much larger than coding RNAs and estimated to be at least four times larger than protein-coding sequences [1]
colorectal cancer (CRC) cell-derived exosomes translocate RPPH1 into macrophages and mediate macrophage M2 polarization LINC00662 promotes M2 polarization by inducing the secretion of WNT3A NORAD knockdown reversed the overexpression of IL-6, IL-8, and tumor necrosis factor-a (TNF-a) pro-inflammatory cytokines in the macrophage cells LncRNA HOTTIP promotes G protein subunit gamma 12 (GNG12) expression, which inhibits M1 and M2 macrophage infiltration Knockdown of GAS5 shows downregulation of M2 surface markers and concomitant increase in M1 markers hypoxia inducible factor-1a (HIF-1a) enhances macrophages recruitment and inducing macrophages toward M2 phenotype
There are several possible directions for future immunotherapeutic strategies for tumors as follows: one is to improve the body’s immune capacity, promote immune activation, such as with macrophages and NK cells to kill tumors, and influence the immune status of the tumor microenvironment (TME); second, to combine multiple targets, such as through the use of traditional radiotherapy modalities and immunotherapy, or multiple different immunotherapies acting in combination, and the detection of various novel markers to identify potentially effective drug targets, such as Long noncoding RNAs (lncRNAs) and Yes-associated protein (YAP), which are closely related to tumors
Summary
The human genome, which typically encodes both coding and non-coding transcripts, contains a large amount of apparently functional but non-coding DNA that is much larger than coding RNAs and estimated to be at least four times larger than protein-coding sequences [1]. CRC cell-derived exosomes translocate RPPH1 into macrophages and mediate macrophage M2 polarization LINC00662 promotes M2 polarization by inducing the secretion of WNT3A NORAD knockdown reversed the overexpression of IL-6, IL-8, and TNF-a pro-inflammatory cytokines in the macrophage cells LncRNA HOTTIP promotes GNG12 expression, which inhibits M1 and M2 macrophage infiltration Knockdown of GAS5 shows downregulation of M2 surface markers and concomitant increase in M1 markers HIF-1a enhances macrophages recruitment and inducing macrophages toward M2 phenotype [19, 28] [20, 29] [22, 30] [23, 31] [47, 48] [34, 49] [45, 50, 51] [43, 52]. In this way can we better advance and expand cancer therapies based on the three conventional and non-conventional therapies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
