RRS1 (Ribosome Biogenesis Regulator 1 Homolog)

Gene expression analysis by qRT-PCR identified notable changes in genes related to these cellular processes, while transcriptome sequencing highlighted five key genes-protein kinase C delta(PRKCD), mitogen-activated protein kinase 3(MAPK3), transient receptor potential cation channel subfamily V member 4(TRPV4), ankyrin 1(ANK1), and phospholipase A2 group VI(PLA2G6)-showing significantly reduced expression after RRS1 knockdown. These findings suggest that RRS1 plays a crucial role in promoting cSCC tumor cell growth and dissemination and highlight its potential as a novel therapeutic target.

In summary, M2 macrophage-derived EVs carrying lncRNA-NEAT1 promote CRC development by modulating the miR-204-5p/RRS1 axis, influencing the cell cycle and apoptosis. These findings provide insights into the tumor-promoting mechanisms of macrophage-derived EVs in CRC.

RRS1 inhibits angiogenesis and cisplatin resistance of lung cancer cells by activating ferroptosis mediated by p53 pathway.

Mechanistically, RRS1 may interact with the AEG-1 to modulate the phosphorylation of AKT at T308 and S473, consequently impeding the activity of c-Myc (p<0.05). To conclude, RRS1 functions as a potential oncogene in breast cancer by leveraging the AEG-1/AKT/c-Myc signaling.

In addition, our findings suggested that RRS1 promoted BC progression by activating the GRP78-mediated phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. In conclusion, this newly discovered RRS1/GRP78 signaling axis provides a molecular and theoretical basis for further exploring the mechanisms of breast cancer invasion and metastasis.

Through the inhibition of the miR-641 level, SNHG1 elevated the level of the downstream target RRS1, thereby fostering BC growth, migration, and invasion while inhibiting apoptosis. These findings suggest that SNHG1 may represent a potential therapeutic target for BC treatment.

The modified phosphoproteome profile of the homozygous mice in combination with human literature suggests a potential signaling pathway from constitutive TSHR signaling and cAMP activation to the activation of ERK/MAPK signaling. This is the first time that a specific mechanism has been identified for a possible involvement of TSH signaling in thyroid carcinoma development.

Low methylation of the RRS1 promoter, RRS1 genomic gain, and hsa-miR-132-3p upregulation in LIHC may promote RRS1 upregulation and thus lead to the development and poor prognosis for LIHC. RRS1 is a promising therapeutic target for LIHC.

The modified phosphoproteome profile of the homozygous mice in combination with human literature suggests a potential signaling pathway from constitutive TSHR signaling and cAMP activation to the activation of ERK/MAPK signaling. This is the first time that a specific mechanism has been identified for a possible involvement of TSH signaling in thyroid carcinoma development.

The modified phosphoproteome profile of the homozygous mice in combination with human literature suggests a potential signaling pathway from constitutive TSHR signaling and cAMP activation, to the activation of ERK/MAPK signaling. This is the first time that a specific mechanism has been identified for a possible involvement of TSH signaling in thyroid carcinoma development.