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Tumor Discovery                                        PTMAP5–hsa-miR-22-3p–KIF2C axis in HCC development



            in HCC require  further  experimental  validation,  this   the R language program for principal component analysis
            pathway will be a central focus of our future research. Our   of the data and carry out in vitro experiments to validate
            study has provided further insights into the mechanism by   our current results. This further research will enable us to
            which the PTMAP5–hsa-miR-22-3p–KIF2C axis operates   further explore the role of the PTMAP5–hsa-miR-22-3p–
            in HCC. Moreover, our results suggest that KIF2C may   KIF2C network in the development of HCC.
            contribute to tumor development by promoting immune
            cell  infiltration into  the  tumor  microenvironment and   5. Conclusion
            upregulating  the  expression  of  immune  checkpoint   Our extensive bioinformatics analyses suggest that the
            markers. However, further foundational and clinical   PTMAP5–hsa-miR-22-3p–KIF2C subnetwork may play
            studies are essential to substantiate these findings.  a crucial role in the emergence and advancement of HCC.
              In our quest to delve deeper into KIF2C’s function in   This regulatory network is implicated in critical biological
            cancer initiation and progression, the TIMER and GEPIA   processes, including cell cycle regulation, oocyte meiosis, and
            databases were employed to examine its expression across   the FOXO signaling pathway. The PTMAP5-hsa-miR-22-3p-
            diverse cancerous and normal tissues. Our discovery using   KIF2C network holds promise as a diagnostic and prognostic
            the TIMER database revealed distinct expression patterns   biomarker for HCC, providing valuable insights into the
            of KIF2C in 16 different cancerous tissue types compared   molecular mechanisms underlying HCC. These findings
            to normal tissues. Similarly, our findings in the GEPIA   could guide future research endeavors aimed at exploring
            database showed variability in KIF2C expression between   the therapeutic and clinical implications of this regulatory
            21 cancer types and corresponding normal tissues. The   network.
            GEPIA  database  indicated  a strong correlation  between
            elevated  KIF2C expression and an increased likelihood   Acknowledgments
            of developing PAAD, KICH, MESO, SKCM, KIRC, ACC,   None.
            KIRP, LUAD, THYM, HCC, PRAD, and LGG. Among
            the 12 cancer types, the highest HR was observed in   Funding
            ACC, with an HR of 9.2, indicating that elevated KIF2C   This  research  was  funded  by  the  Natural  Science
            expression significantly contributes to poor prognosis in   Foundation  of  Guangxi  Province  (grant  number:
            ACC patients.
                                                               2017GXNSFAA198063) and the Basic Medical Science and
              We further explored  the associations  between  KIF2C   Technology Innovation Training Fund Project of Guangxi
            and MHC molecules, immunomodulators, chemokines,   Medical University (grant number: GXMUBMSTCF-G15).
            and receptors using the TISIDB database, as well as the
            relationships between  KIF2C expression levels and pan-  Conflict of interest
            cancer immune and molecular subtypes. In HCC, KIF2C   The authors declare that they have no competing interests.
            was found to be associated with most immunomodulators,
            chemokines, and receptors, with the strongest correlation   Author contributions
            observed  with  the  chemokine  CCL14  (Rho  =  −0.644,
            P = 4.28e−12). In addition, we noted variations in KIF2C   Conceptualization: All authors
            expression across different human cancer types, particularly   Investigation: Qing Deng, Yuanchao Wei, Jiali Meng
            within immune and molecular subtypes. KIF2C was found   Methodology: Xiaolong Li
            to be involved in ACC, BLCA, BRCA, CESC, COAD,     Writing – original draft: Qing Deng, Yuanchao Wei, Jiali
            ESCA, HNSC, LGG, HCC, LUAD, LUSC, MESO, OV,           Meng
            PAAD, PRAD, READ, SARC, SKCM, and STAD. Similarly,   Writing – review & editing: Xiaolong Li, Qing Deng
            significant KIF2C expression was observed in uterine corpus   Ethics approval and consent to participate
            endometrial carcinoma and 20 other cancers. Among the
            different molecular subtypes,  KIF2C showed significant   Not applicable.
            expression in 13 cancers. These findings underscore the
            potential clinical value of KIF2C in cancer treatment and   Consent for publication
            highlight its role as a potential therapeutic target.  Not applicable.
              However, it is necessary to acknowledge the limitations   Availability of data
            of this work. Our data processing methods were relatively
            simple, and no  in vitro experiments were performed to   The data were derived from the GSE87630 and GSE45267
            validate the results. In our future work, we plan to use   datasets of the GEO database.


            Volume 3 Issue 3 (2024)                         21                                doi: 10.36922/td.2846
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