The inhibition roles of RAB23 gene in granulosa cell proliferation and progesterone synthesis of hen ovarian prehierarchical follicles.

1. The proliferation of granulosa cells is vital for the development and recruitment of hen ovarian prehierarchical follicles (PF). The RAB23 protein is a member of the Rab family, belonging to the GTPase family. This study studied the regulatory roles of the RAB23 gene in PF.2. The expression of RAB23 was significantly increased in granulosa cells (GC) during PF growth and was highest in GC at 6-8 mm diameter (p < 0.05). The RAB23 protein was mainly expressed in the GC, oocytes (OC) as well as somatic cells (SC) of the PF.3. The mRNA expression of FSHR, CCND1,CYP11A1, StAR and HSD3B1 was significantly increased in the siRNA RAB23 group (p < 0.05). Additionally, protein expression of FSHR, CCND1, CYP11A1, HSD3B1 was significantly increased (p < 0.05) after GC were transfected with RAB23-specific siRNA. Protein expression of StAR in the siRNA RAB23 group was numerically higher than that in the positive control (PC) and negative control (NC) groups. The GC proliferation rate and progesterone synthesis of the prehierarchical follicles in hen ovaries were markedly increased in vitro (p < 0.05).4.This study revealed that RAB23 might play an inhibitory role in GC proliferation and progesterone synthesis during the prehierarchical follicles development in vitro.

Silencing of Rab23 by siRNA inhibits ultraviolet B-induced melanogenesis via downregulation of PKA/CREB/MITF.

Recent investigations have shown that the Rab family of GTPases is associated with all aspects of melanogenesis. However, the effect of Rab23, which localizes to the plasma membrane and regulates the endocytic pathway within eukaryotic cells, in melanogenesis has not been reported. To understand the role of Rab23 in UVB-induced melanogenesis, we evaluated changes in the level of melanin, activity of tyrosinase and levels of melanogenesis-related proteins such as microphthalmia transcription factor and tyrosinase-related protein-1 (TRP-1) and the melanosome transport-related protein complex Rab27a-melanophilin-myosin Va after the downregulation of Rab23 in B16F10 and SK-MEL-2 cells with or without UVB irradiation. Our results showed that downregulating Rab23 reduced the melanin level and tyrosinase activity and inhibited the expression of proteins involved in UVB-induced melanogenesis. Rab23 colocalized with mature melanosomes marked with TRP-1. Furthermore, downregulating Rab23 induced the abnormal accumulation of melanosomes around the nucleus. We demonstrated that the downregulation of Rab23 inhibited melanin synthesis and melanosome transport by decreasing the PKA/CREB/MITF pathway, which is the key regulator of UVB-induced melanogenesis.

Carpenter syndrome in a patient from Tanzania.

Carpenter syndrome (acrocephalopolysyndactyly type II) is a rare autosomal recessive disorder. It was clinically diagnosed in a female baby with polysyndactyly and craniosynostosis in a referral clinic in Northern Tanzania. In the RAB23 gene, a previously described homozygous variant c.82C>T p.(Arg28*) was detected that results in a premature stop codon. Both parents were demonstrated to be heterozygous carriers of this variant. Herewith, its pathogenicity is proved. A literature search suggests this is the first molecularly confirmed case of Carpenter syndrome in continental Africa.

lncRNA OSER1-AS1 acts as a ceRNA to promote tumorigenesis in hepatocellular carcinoma by regulating miR-372-3p/Rab23 axis.

Long non-coding RNAs (lncRNAs) are crucial regulators of tumorigenesis and progression in human cancer, including hepatocellular carcinoma (HCC). However, the role of most lncRNAs that are dysregulated in HCC remains to be elucidated. Here, we investigated the role of OSER1-AS1 in the progression of HCC. The results of database and qRT-PCR analysis demonstrated that OSER1-AS1 was highly expressed in HCC tissues and the high expression of OSER1-AS1 was closely associated with larger tumor size, advanced tumor stages, lower disease free survival and overall survival of HCC patients. OSER1-AS1 knockdown significantly inhibited the proliferation, invasion and migration of HCC cells, and induced the apoptosis. In addition, the dual luciferase reporter assay directly demonstrated that OSER1-AS1 functioned as a molecular sponge for miR-372-3p to promote Rab23 expression. Moreover, the results of immunohistochemistry and western blot analysis showed that Rab23 was highly expressed in HCC tissues, and the high expression of Rab23 was closely associated with the poor overall survival of HCC patients. Immunofluorescence assay also found the subcellular localization of Rab23 in HCC cells. Rab23 was obviously downregulated in cells that were transfected with miR-372-3p mimics. MiR-372-3p mimics significantly inhibited the proliferation and invasion of HCC cells). Rab23 restoration partially reversed miR-372-3p-induced tumor suppressive effects on HCC cells. In conclusion, we found that OSER1-AS1 acted as a ceRNA to sponge miR-372-3p, thereby positively regulating the Rab23 expression and ultimately acting as a tumor suppressor gene in HCC progression.

miR-384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23.

microRNAs (miRNAs) are noncoding, short, and endogenous RNAs that play crucial roles in tumor progression at the post-transcriptional level. Here, we studied the role of miR-384 in the pathogenesis of renal cell carcinoma (RCC). We demonstrated that miR-384 expression was downregulated in the RCC specimens compared with nontumor specimens. Moreover, we showed that RAB23 expression was upregulated in the RCC tissues compared with nontumor tissues. Furthermore, we demonstrated that low expression of miR-384 was correlated with high levels of RAB23 in RCC tissues. We also demonstrated that the RAB23 was a direct target gene of miR-384 in RCC cells. In addition, overexpression of miR-384 suppressed RCC cell proliferation, cell cycle, and cell migration. Furthermore, ectopic expression of RAB23 promoted RCC cell proliferation, cell cycle, and cell migration. These data suggested that miR-384 played a tumor suppressor microRNA in the development of RCC partly through inhibiting RAB23 expression.

Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p.

BACKGROUND: CircRNA myosin light chain kinase (circRNA MYLK) has been shown to promote the progression of various tumor diseases. The purpose of this study was to explore the potential molecular mechanism of circMYLK in hepatocellular carcinoma (HCC). METHODS: The quantitative Real-Time PCR (qRT-PCR) was used to measure the expressions of circMYLK, miR-362-3p and Rab23 in HCC tissues and cell lines. Huh7 and Hep3B cells were selected to explore the role of circMYLK in proliferation, invasion and migration of HCC cells in vitro. The interaction among circMYLK, miR-362-3p and Rab23 was investigated by biological information and dual luciferase gene reporter assay. The effect of circMYLK on HCC tumor growth in vivo was studied in a tumor xenograft model in mice. RESULTS: CircMYLK was highly expressed in HCC tissues and cell lines, which was associated with poor prognosis in HCC patients. In addition, knockdown of circMYLK remarkably inhibited the proliferation, invasion, and migration of Huh7 and Hep3B cells. MiR-362-3p was a direct target of circMYLK, and Rab23 was a direct target gene of miR-362-3p. Meanwhile, circMYLK was negatively correlated with the expression of miR-362-3p and positively correlated with Rab23 expression. Moreover, either overexpressed miR-362-3p or silencing Rab23 could observably suppress the enhanced proliferation, invasion, and migration induced by circMYLK in Huh7 and Hep3B cells. Finally, knockdown of circMYLK and overexpressed miR-362-3p could suppress the expression of Rab23, thus inhibiting the growth and proliferation of Hep3B cells in vivo. CONCLUSION: circMYLK promotes the occurrence and development of HCC by regulating the miR-362-3p/Rab23 axis, which provides a novel direction and theoretical basis for the early diagnosis and treatment of HCC.

MiR-429 regulates the metastasis and EMT of HCC cells through targeting RAB23.

Accumulating documents have revealed that microRNAs (miRNAs) play critical roles in the development and progression of tumors. MiR-429 has been reported to be involved in regulating various cellular processes. However, its biological role and underlying mechanism in hepatocellular carcinoma (HCC) still need to be further studied. The present study aimed to investigate the function of miR-429 in the progression of HCC. In terms of this paper, it was found that miR-429 was down-regulated in HCC tissues and cells. After being transfected with miR-429 mimics, miR-429 decreased the migratory capacity and reversed the EMT to MET in HCC cells. RAB23 was confirmed as a target of miR-429. Rescue assays further verified that the function of miR-429 in HCC cells was exerted through targeting RAB23. In general, it was concluded that the signal pathway miR-429/RAB23 might be a potential target for HCC treatment.

A role for Rab23 in the trafficking of Kif17 to the primary cilium.

The small GTPase Rab23 is an antagonist of sonic hedgehog (Shh) signaling during mouse development. Given that modulation of Shh signaling depends on the normal functioning of the primary cilium, and overexpression of Evi5L, a putative Rab23 GTPase-activating protein (GAP), leads to reduced ciliogenesis, Rab23 could have a role at the primary cilium. Here, we found that wild-type Rab23 and the constitutively active Rab23 Q68L mutant were enriched at the primary cilium. Therefore, we tested the role of Rab23 in the ciliary targeting of known cargoes and found that ciliary localization of the kinesin-2 motor protein Kif17 was disrupted in Rab23-depleted cells. Co-immunoprecipitation and affinity-binding studies revealed that Rab23 exists in a complex with Kif17 and importin ß2 (the putative Kif17 ciliary import carrier), implying that Kif17 needs to bind to regulatory proteins like Rab23 for its ciliary transport. Although a ciliary-cytoplasmic gradient of nuclear Ran is necessary to regulate the ciliary transport of Kif17, Rab23 and Ran appear to have differing roles in regulating the ciliary entry of Kif17. Our findings have uncovered a hitherto unknown effector of Rab23 and demonstrate how Rab23 could mediate the transport of Kif17 to the primary cilium.

Rab23 is overexpressed in human bladder cancer and promotes cancer cell proliferation and invasion.

Rab23 overexpression has been implicated in several human cancers. However, its expression pattern and biological roles in human bladder cancer have not been elucidated. In this study, we examined Rab23 expression in 93 bladder cancer specimens and analyzed its correlation with clinicopathological parameters. We found that Rab23 was overexpressed in 45 of 93 (48.3 %) cancer specimens. Significant association was found between Rab23 overexpression and tumor invasion depth (p = 0.0027). Rab23 overexpression also negatively correlated with FGFR3 protein expression (p = 0.021). We found that Rab23 expression was lower in normal bladder transitional cell line SV-HUC-1 than in bladder cancer cell lines BIU-87, 5637, and T24. We knocked down Rab23 expression in T24 cancer cells and transfected a Rab23 plasmid in the BIU-87 cell line. Rab23 depletion inhibited cell growth rate and invasion, while its overexpression resulted in increased cell growth and invasion. In addition, we demonstrated that Rab23 depletion decreased and its transfection upregulated expression of cyclin E, c-myc, and MMP-9. Furthermore, we showed that Rab23 knockdown inhibited NF-κB signaling and its overexpression upregulated NF-κB signaling. BAY 11-7082 (NF-κB inhibitor) partly inhibited the effect of Rab23 on cyclin E and MMP-9 expression. In conclusion, the present study demonstrated that Rab23 overexpression facilitates malignant cell growth and invasion in bladder cancer through the NF-κB pathway.

Rab23 is overexpressed in human astrocytoma and promotes cell migration and invasion through regulation of Rac1.

Rab23 overexpression has been implicated in several human cancers. However, its biological roles and molecular mechanism in astrocytoma have not been elucidated. The aim of this study is to explore clinical significance and biological roles of Rab23 in astrocytoma. We observed negative Rab23 staining in normal astrocytes and positive staining in 39 out of 86 (45 %) astrocytoma specimens using immunohistochemistry. The positive rate of Rab23 was higher in grades III and IV (56.5 %, 26/46) than grades I + II astrocytomas (32.5 %, 13/40, p < 0.05). Transfection of Rab23 plasmid was performed induced A172 cell proliferation, colony formation, invasion, and migration, while Rab23 depletion with siRNA reduced these abilities of U87 cells. In addition, we found that Rab23 transfection upregulated while its depletion reduced Rac1 activity. Treatment of transfected cells with a Rac1 inhibitor decreased Rac1 activity and invasion. In conclusion, Rab23 serves as an important oncoprotein in human astrocytoma by regulating cell invasion and migration through Rac1 activity.

Rab23 activities and human cancer-emerging connections and mechanisms.

Unlike founding members of the Ras superfamily of small GTPases that are prominently known for oncogenic signaling, members of the Rab subfamily are key regulators of cellular membrane traffic. However, a number of Rabs have in recent years also been strongly implicated as tumorigenic or metastatic biomarkers. Rab23 is an emerging example whose differential expression in tumor cells and functional association with proliferation and invasiveness is attracting attention as a useful cancer marker and a potential therapeutic target. Rab23 is ubiquitously expressed but appears to be particularly enriched in the adult brain. It has important developmental functions in vertebrates and has been shown to modulate Sonic hedgehog (Shh) and Nodal signaling. Although its exact cellular role in membrane traffic regulation remains elusive, its known role in Shh signaling, in conjunction with several recent findings, has clearly implicated a role for Rab23 in transport processes to the primary cilium. In this review, we summarize what is currently known about Rab23 as a cancer marker and discuss possible mechanism by which this Rab GTPase may act as an oncogenic or metastatic driver, while exhibiting tumor suppressive activity in some cases.

Rab23 regulates Nodal signaling in vertebrate left-right patterning independently of the Hedgehog pathway.

Asymmetric fluid flow in the node and Nodal signaling in the left lateral plate mesoderm (LPM) drive left-right patterning of the mammalian body plan. However, the mechanisms linking fluid flow to asymmetric gene expression in the LPM remain unclear. Here we show that the small GTPase Rab23, known for its role in Hedgehog signaling, plays a separate role in Nodal signaling and left-right patterning in the mouse embryo. Rab23 is not required for initial symmetry breaking in the node, but it is required for expression of Nodal and Nodal target genes in the LPM. Microinjection of Nodal protein and transfection of Nodal cDNA in the embryo indicate that Rab23 is required for the production of functional Nodal signals, rather than the response to them. Using gain- and loss-of function approaches, we show that Rab23 plays a similar role in zebrafish, where it is required in the teleost equivalent of the mouse node, Kupffer׳s vesicle. Collectively, these data suggest that Rab23 is an essential component of the mechanism that transmits asymmetric patterning information from the node to the LPM.

Prenatal findings in carpenter syndrome and a novel mutation in RAB23.

Carpenter syndrome is caused by mutations of the RAB23 gene. To date, 12 distinct mutations have been identified among 34 patients from 26 unrelated families. We report on the prenatal findings in a fetus with Carpenter syndrome with a novel RAB23 mutation. Cystic hygroma, bowed femora, abnormal skull shape and a complex heart defect were seen on ultrasound scan, and Carpenter syndrome was diagnosed at birth. Craniosynostosis and preaxial hexadactyly of the feet were retrospectively detectable on the fetal CT scan. Sequencing of RAB23 identified a homozygous mutation leading to skipping of exon 6 and premature termination codon (c.481G>C; p.Val161Leufs*16). This observation illustrates the difficulty of prenatal ultrasound diagnosis of Carpenter syndrome. To our knowledge, this diagnosis was suggested on ultrasound scan in only one prior patient, although in five other patients abnormal skull shape and variable findings, mainly limb anomalies including bowed femora in one case, were described during the pregnancy. Heart defect and bowed femora are rare postnatal findings. The diagnosis of Carpenter syndrome should therefore be considered on prenatal imaging in cases of bowed femora and/or cardiac defect associated with abnormal skull shape.

Downregulation of Rab23 inhibits hepatocellular carcinoma by repressing SHH signaling pathway.

Hepatocellular carcinoma (HCC) is the sixth most common malignant tumors and the third leading cause of cancer-related death worldwide. As an oncogene, Rab23 has been shown to be significantly related to the growth and migration of hepatocellular carcinoma in both in vitro and in vivo studies, but its underlying mechanism remains obscure. In the present study, we examined the effect of inhibiting Rab23 expression on the pathological progression of HCC. The correlation between liver Rab23 gene expression and survival probability in human HCC patients was analyzed using the TCGA database and CPTAC database. Rab23 knockdown hepatocellular carcinoma cell line was generated through lentiviral transduction, then we established a nude HCC xenograft model by subcutaneously implanting the transfected cells. The analysis of gene and protein expression was carried out using Western blot or RT-qPCR, respectively. Flow cytometry analysis was used to detect the level of apoptosis. The expression levels of key proteins involved in the Sonic Hedgehog (SHH) signaling pathway were assessed. The results showed that HCC patients with low levels of hepatic Rab23 mRNA and protein had a better survival tendency than those with higher levels of Rab23. Cell proliferations were reduced and apoptosis levels were increased after Knocking down Rab23 in HCC cell lines. Furthermore, in vivo studies have demonstrated that suppression of the Rab23 gene results in decreased tumor size, proliferation rate, and reduced levels of SHH-related proteins Smoothened and GLI-1. The above results suggest that Rab23 is involved in the pathological progression of HCC as an important regulator of the SHH signaling pathway, which also provides an important research basis for new therapeutic strategies for HCC.

A Rare Case of Carpenter Syndrome and Its Unique Association With Chronic Kidney Disease.

Carpenter syndrome, characterized by RAB23 mutations, is a rare autosomal recessive disorder distinguished by unique features such as craniofacial anomalies, congenital heart disease, brachydactyly, and obesity. This syndrome's rarity, with an estimated prevalence of one in a million births, poses diagnostic challenges due to its diverse clinical spectrum. Notably, this case report highlights an unusual association of Carpenter syndrome with chronic kidney disease (CKD), underscoring the need for further exploration into the syndromic interplay and shared genetic pathways. The distinctive manifestation of CKD in the context of Carpenter syndrome adds a novel dimension, emphasizing the importance of timely diagnosis and comprehensive care. Further research is warranted to unravel the intricate genetic and molecular pathways underlying the syndrome's diverse manifestations, shedding light on potential shared mechanisms and paving the way for targeted interventions and enhanced patient care.

Comprehensive bioinformatics analysis reveals the oncogenic role of FoxM1 and its impact on prognosis, immune microenvironment, and drug sensitivity in osteosarcoma.

Osteosarcoma, a highly malignant bone tumor primarily affecting adolescents, presents a significant challenge in cancer therapy due to its resistance to chemotherapy. This study explores the multifaceted impact of the transcription factor FoxM1 on osteosarcoma, shedding light on its pivotal role in tumor progression, immune microenvironment modulation, and drug response. Utilizing publicly available datasets from the Gene Expression Omnibus (GEO) and Therapeutically Applicable Research To Generate Effective Treatments (TARGET) databases, we conducted an in-depth bioinformatics analysis. Our findings illuminate the far-reaching implications of FoxM1 in osteosarcoma, emphasizing its significance as a potential therapeutic target. Differential expression analysis and Gene Set Enrichment Analysis (GSEA) revealed FoxM1's influence on critical pathways related to apoptosis, cell cycle regulation, and DNA repair. Notably, FoxM1 expression correlated with poor clinical outcomes in osteosarcoma patients, highlighting its prognostic relevance. Additionally, FoxM1 was found to modulate the immune microenvironment within tumor tissues, impacting immune cell infiltration, immunomodulators, immune checkpoints, and chemokines. Furthermore, a prognostic model based on FoxM1-coexpressed genes demonstrated its effectiveness in predicting patient survival. Drug sensitivity analysis indicated FoxM1's association with drug response, potentially guiding personalized treatment approaches. Hub gene screening identified RAB23 as a key target regulated by FoxM1, with RAB23 shown to influence osteosarcoma cell growth. This study also confirmed FoxM1's overexpression in osteosarcoma tissues compared to normal tissues, and its association with clinicopathological characteristics, including clinical stage, pathological type, and lung metastasis. In conclusion, FoxM1 emerges as a central player in the pathogenesis of osteosarcoma, impacting gene expression, immune responses, and therapeutic outcomes. This comprehensive analysis deepens our understanding of FoxM1's role in osteosarcoma and offers potential avenues for improved diagnosis and treatment.

MicroRNA-367-3p directly targets RAB23 and inhibits proliferation, migration and invasion of bladder cancer cells and increases cisplatin sensitivity.

OBJECTIVES: This study investigated the biological role of miR-367-3p upregulation in bladder cancer and verified the mutual relation between miR-367-3p and RAB23. MATERIALS AND METHODS: Expression levels of miR-367-3p were determined by RT-qPCR in bladder cancer cell lines and human bladder cancer tissues. The effects of miR-367-3p on proliferation, migration and invasion were evaluated by cell colony formation assays, wound healing assays and trans-well assays, respectively. The effects of miR-367-3p and RAB23 on cisplatin sensitivity of bladder cancer cells were assessed by CCK-8 assay. The expression of its target-RAB23 was determined by western blotting in T24, 5637. Plasmids used in dual-luciferase assays were constructed to confirm the action of miR-367-3p on downstream target-RAB23 in T24 cells. And also, the role of miR-367-3p in tumorigenesis was also confirmed in nude mouse models. RESULTS: The downregulation of miR-367-3p was observed in human bladder cancer tissues. MiR-367-3p downregulation positively correlated with tumor stage and tumor grade. MiR-367-3p overexpression in T24, 5637 cells suppressed the proliferation, migration, and invasion of bladder cancer cells in vitro while decreasing IC50 values under T24 and 5637 cisplatin treatment conditions. RAB23 was shown to be upregulated in bladder cancer tissues and cell lines. MiR-367-3p directly bound to the 3' UTR of RAB23 in T24 cells. RAB23 was potentially accounted for the aforementioned functions of miR-367-3p. Tumor formation experiments in nude mouse models confirmed that overexpression of miR-367-3p could inhibit tumor growth and invasion in vivo. CONCLUSIONS: miR-367-3p acts as a tumor suppressor in bladder cancer by downregulating RAB23 signaling. We conjecture that miR-367-3p-mediated downregulation of RAB23 expression may be a new therapeutic strategy for bladder cancer treatment.

RAB23 regulates musculoskeletal development and patterning.

RAB23 is a small GTPase which functions at the plasma membrane to regulate growth factor signaling. Mutations in RAB23 cause Carpenter syndrome, a condition that affects normal organogenesis and patterning. In this study, we investigate the role of RAB23 in musculoskeletal development and show that it is required for patella bone formation and for the maintenance of tendon progenitors. The patella is the largest sesamoid bone in mammals and plays a critical role during movement by providing structural and mechanical support to the knee. Rab23 -/- mice fail to form a patella and normal knee joint. The patella is formed from Sox9 and scleraxis (Scx) double-positive chondroprogenitor cells. We show that RAB23 is required for the specification of SOX9 and scleraxis double-positive patella chondroprogenitors during the formation of patella anlagen and the subsequent establishment of patellofemoral joint. We find that scleraxis and SOX9 expression are disrupted in Rab23 -/- mice, and as a result, development of the quadriceps tendons, cruciate ligaments, patella tendons, and entheses is either abnormal or lost. TGFß-BMP signaling is known to regulate patella initiation and patella progenitor differentiation and growth. We find that the expression of TGFßR2, BMPR1, BMP4, and pSmad are barely detectable in the future patella site and in the rudimentary tendons and ligaments around the patellofemoral joint in Rab23 -/- mice. Also, we show that GLI1, SOX9, and scleraxis, which regulate entheses establishment and maturation, are weakly expressed in Rab23 -/- mice. Further analysis of the skeletal phenotype of Rab23 -/- mice showed a close resemblance to that of Tgfß2 -/- mice, highlighting a possible role for RAB23 in regulating TGFß superfamily signaling.

Biomarker of Pulmonary Inflammatory Response in LUAD: miR-584-5p Targets RAB23 to Suppress Inflammation Induced by LPS in A549 Cells.

BACKGROUND: Pulmonary inflammatory response (PIR) is one of the prognostic risk factors of lung adenocarcinoma (LUAD), with a high mortality rate. OBJECTIVES: This study aims to investigate prognostic microRNA (miRNA) to improve clinical prognosis prediction and postoperative inflammation treatment in LUAD patients. METHODS: About 201 differentially expressed microRNAs (DE-miRNAs) in LUAD were mined by differential analysis. Univariate/multivariate Cox analyses established and validated prognostic risk miRNAs in TCGA-LUAD. KEGG and GO were used to link risk signatures and biological functions. After 48 hours of exposure to 50 ng/mL LPS, the miR-584-5p/RAB23 regulatory network was verified in qRT-PCR, Western Blotting, and the Luciferase Reporter Assay in A549 cells. RESULTS: MiR-584-5p and miR-101-3p were validated as riskscore correlated with LUAD patients' 1-year survival (p < 0.001) and participate in multiple inflammation-related pathways. RAB23, a RAS oncogene, is involved in inflammatory MAPK signaling. Evidence suggests that miR-584-5p regulates inflammation in LUAD by targeting RAB23. A549 cells were transfected with the mimic and inhibitor of miR-584-5p, confirming the negative regulatory relationship between miR-584-5p and RAB23. In the A549 induced by LPS, either over-expression of miR-584-5p or knock-down of RAB23 expression decreased the expression of inflammatory factors and increased cell viability. CONCLUSION: Prognostic-related risk miR-584-5p can regulate the expression of RAB23 at both the mRNA and protein levels, thereby influencing the development of a PIR in LUAD. This will have significant implications for the clinical prognosis prediction and therapy decision-making of LUAD patients with PIR.