| 1994 |
Rat RPS15A (S15a) is a component of the 40S ribosomal subunit, consists of 129 amino acids (NH2-terminal methionine removed post-translationally), and is encoded by a multi-copy gene family (10–15 copies) producing an ~650 nt mRNA. |
cDNA cloning, nucleotide sequencing, Southern/Northern blotting |
Biochemical and biophysical research communications |
High |
8185605
|
| 2004 |
Human RPS15A (S15a) expression is upregulated by hepatitis B virus X antigen (HBxAg); overexpression of S15a stimulates cell growth, colony formation in soft agar, and tumor formation in SCID mice, implicating it in translational integrity and HCC development. |
PCR-select cDNA subtraction, Northern/Western blotting, soft-agar colony formation, SCID mouse xenograft |
Molecular carcinogenesis |
Medium |
15108328
|
| 2013 |
shRNA-mediated knockdown of RPS15A inhibits hepatic cancer cell (HepG2, Bel7404) proliferation, impairs colony formation, and arrests cells at G0/G1 phase, demonstrating a required role in cell cycle progression. |
Lentiviral shRNA knockdown, MTT/colony formation assays, flow cytometry cell-cycle analysis |
Gene |
Medium |
24334120
|
| 2015 |
RPS15A knockdown in glioblastoma cells (U87, U251) decreases p-Akt levels, arrests cells at G0/G1, inhibits proliferation and migration in vitro, and suppresses tumor growth in nude mice, placing RPS15A upstream of the AKT pathway. |
Lentiviral RNAi, Western blot (p-Akt), MTT, wound-healing, transwell migration, nude mouse xenograft |
Tumour biology |
Medium |
26537582
|
| 2016 |
RPS15A knockdown in glioblastoma U251 cells inhibits growth, induces G0/G1 arrest, triggers apoptosis, decreases Bcl-2 protein, and activates caspase-3 and PARP cleavage, defining a pro-survival/anti-apoptotic mechanism. |
Lentiviral RNAi, MTT, colony formation, flow cytometry, Western blot (Bcl-2, caspase-3, PARP) |
World journal of surgical oncology |
Medium |
27130037
|
| 2016 |
In lung adenocarcinoma cells, RPS15A knockdown inhibits growth, induces apoptosis, and activates the p53 signaling pathway as revealed by gene expression microarray, suggesting RPS15A suppresses p53 activity. |
Lentiviral shRNA, gene expression microarray, flow cytometry |
PeerJ |
Medium |
26989627
|
| 2017 |
RPS15A promotes tumor angiogenesis in hepatocellular carcinoma by enhancing Wnt/β-catenin-mediated FGF18 expression in HCC cells; secreted FGF18 then binds FGFR3 on endothelial cells to activate AKT and ERK, stimulating angiogenesis. |
HCC cell overexpression/knockdown, HUVEC co-culture paracrine angiogenesis assay, reporter assays, Western blot, nude mouse xenograft |
Oncogene |
High |
29242604
|
| 2017 |
miR-29 family members directly bind the 3′-UTR of RPS15A mRNA (validated by luciferase assay) and reduce RPS15A protein, consequently downregulating cyclin A, cyclin D1 and upregulating p21, thereby regulating cell cycle in HCC. |
Luciferase 3′-UTR reporter assay, Western blot, cell cycle analysis |
International journal of clinical and experimental pathology |
Medium |
31966655
|
| 2019 |
RPS15A activates the NF-κB pathway in gastric cancer by inducing Akt/IKK-β signaling, leading to phosphorylation and nuclear translocation of p65; both Akt inhibitor LY294002 and IKK inhibitor Bay117082 block p65 nuclear translocation induced by RPS15A overexpression, placing RPS15A upstream of Akt/IKK-β/NF-κB. |
Overexpression/knockdown, NF-κB reporter assay, Western blot (p-p65, nuclear fractionation), pharmacological inhibitors, in vivo xenograft |
Journal of cellular and molecular medicine |
High |
30661291
|
| 2019 |
RPS15A is a direct target of miR-519d-3p (validated by luciferase reporter); RPS15A knockdown downregulates β-catenin and blocks Wnt/β-catenin signaling in pancreatic cancer cells; restoration of RPS15A reverses the antitumor effect of miR-519d-3p. |
Luciferase 3′-UTR reporter assay, Western blot, cell proliferation assay, rescue experiment |
Chemico-biological interactions |
Medium |
30831090
|
| 2019 |
RPS15A knockdown in breast cancer MDA-MB-231 cells suppresses phosphorylation of ERK1/2, Bad, and Chk1, and activates caspase-3/-7, indicating RPS15A inhibits apoptosis via the ERK1/2/Bad/Chk1 axis. |
Lentiviral shRNA, Western blot (p-ERK1/2, p-Bad, p-Chk1), caspase-3/-7 activity assay |
Journal of cellular biochemistry |
Medium |
31535410
|
| 2019 |
miR-147b directly targets RPS15A (validated by luciferase reporter), negatively regulates its expression in NSCLC cells, and thereby downregulates Wnt/β-catenin signaling; overexpression of RPS15A partially reverses the antitumor effect of miR-147b. |
Luciferase 3′-UTR reporter assay, Western blot, functional rescue experiment |
Clinical and experimental pharmacology & physiology |
Medium |
31665807
|
| 2021 |
RPS15A knockdown in colorectal cancer RKO cells induces apoptosis via regulation of BIRC3, p38 MAPK, and Chk1, and causes G2/M arrest, as identified by KEGG pathway analysis of 785 differentially expressed genes and confirmed by Western blot. |
Lentiviral shRNA, microarray/KEGG pathway analysis, Western blot, flow cytometry, nude mouse xenograft |
European review for medical and pharmacological sciences |
Medium |
34156695
|
| 2022 |
PSMC2 promotes RPS15A expression by competitively binding hsa-let-7c-3p; elevated RPS15A in turn activates the mTOR pathway; mTOR inhibitor Torin1 partially reverses RPS15A-overexpression-induced proliferation, placing RPS15A downstream of PSMC2/let-7c-3p and upstream of mTOR. |
GeneChip analysis, dual-luciferase reporter assay, RPS15A overexpression rescue, Torin1 pharmacological inhibition, Western blot |
Oncogenesis |
Medium |
35256584
|
| 2023 |
FBXL18, an E3 ubiquitin ligase, promotes K63-linked ubiquitination of RPS15A, enhancing its protein stability; stabilized RPS15A increases SMAD3 levels and promotes its nuclear translocation, driving HCC cell proliferation; knockdown of RPS15A or SMAD3 suppresses FBXL18-mediated proliferation. |
Co-IP, ubiquitination assay (K63-linkage specific), Western blot (SMAD3, nuclear fractionation), FBXL18 transgenic mice, knockdown rescue experiments |
Hepatology communications |
High |
37378633
|
| 2023 |
FOXN3 transcription factor binds to the RPS15A promoter at two specific sites (−1588/−1581 and −1476/−1467) and represses its transcriptional expression, as shown by dual-luciferase assay and ChIP; RPS15A overexpression reverses FOXN3-mediated suppression of ovarian cancer malignant behaviors. |
Dual-luciferase promoter assay, ChIP, overexpression rescue experiments |
Human cell |
Medium |
37016167
|
| 2023 |
miR-147b directly targets RPS15A (validated by luciferase reporter) in prostate cancer cells; RPS15A is downregulated in neuroendocrine prostate cancer cells and its expression is inversely correlated with NE markers; overexpression of miR-147b reduces cyclin D1 and elevates p27kip1, while RPS15A inhibition contributes to neuroendocrine differentiation. |
Luciferase reporter assay, Western blot, miRNA mimic/inhibitor experiments, RT-PCR |
The Prostate |
Medium |
37069746
|
| 2025 |
RPS15A knockdown in B-ALL cells impairs ribosomal biogenesis by suppressing synthesis and processing of pre-rRNA, 18S rRNA, 28S rRNA, and 5.8S rRNA; this disrupts nucleolar architecture (displaces NPM1 and FBL), induces nucleolar stress, and activates p53/p21 signaling, causing cell cycle arrest and apoptosis; p53 knockdown after RPS15A KD rescues rRNA biogenesis, cell cycle progression, and inhibits apoptosis. |
Lentiviral shRNA, immunofluorescence (NPM1/FBL localization), RT-PCR (rRNA processing), flow cytometry, Western blot (p53/p21), p53 rescue experiment |
Biochemical and biophysical research communications |
High |
40239541
|
| 2025 |
GGCT physically interacts with RPS15A (shown by co-IP and LC-MS/MS) and promotes RPS15A protein stability; RPS15A knockdown activates p53, which represses SLC7A11, reducing GSH synthesis and promoting ferroptosis in papillary thyroid cancer cells; RPS15A overexpression reverses GGCT-knockdown-induced ferroptosis. |
Co-immunoprecipitation, LC-MS/MS, Western blot, ferroptosis assays (MDA, ROS), rescue overexpression |
Cancer science |
Medium |
40044122
|
| 2025 |
lncRNA RHPN1-AS1 physically interacts with RPS15A protein and stabilizes it in hypoxic HCC cells; elevated RPS15A then activates β-catenin signaling to promote proliferation and invasion; silencing RPS15A attenuates RHPN1-AS1-induced aggressiveness and β-catenin activation. |
RNA-protein pull-down/interaction assay, Western blot (β-catenin), knockdown rescue, xenograft tumor model |
Medical oncology |
Medium |
41026296
|