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Research Paper|Volume 15, Issue 23|pp 13944—13960

SEMA3G, downregulated by ncRNAs, correlates with favorable prognosis and tumor immune infiltration in kidney renal clear cell carcinoma

Jian Yuan1, Guorong Yuan2
  • 1Department of Medical Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China
  • 2Cancer Center, Department of Medical Oncology, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China
Received: September 8, 2023Accepted: October 29, 2023Published: December 8, 2023
https://doi.org/10.18632/aging.205277

Copyright: © 2023 Yuan and Yuan. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Kidney renal clear cell carcinoma (KIRC), relatively aggressive subtype of renal cell carcinoma, lacks of effective targets and promising biomarkers. Recently, although the function and immune correlation of semaphorin 3G (SEMA3G) in cancer draw more and more attention, its specific role and mechanism in KIRC are still not fully understood. In this work, we firstly conducted pan-cancer expression and survival bioinformatic analysis for SEMA3G and showed that SMEA3G might be a potential tumor suppressor and favorable prognostic biomarker in KIRC. Next, upstream noncoding RNA (ncRNA) regulatory mechanism of SEMA3G in KIRC was explored. By performing a series of in silico analyses, we identified that TBX2-AS1-miR-146a/b-5p axis was partially responsible for SEMA3G downregulation in KIRC. Furthermore, we also confirmed significant correlation of SEMA3G expression with tumor immune infiltration levels, expression of biomarkers of immune cells or immune checkpoints in KIRC. Taken together, the current data elucidated that ncRNA-caused downregulation of SEMA3G markedly linked to favorable prognosis and tumor immune infiltration in KIRC.