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RRS1 (human regulator of ribosome synthesis 1), an essential nuclear protein involved in ribosome biogenesis, is overexpressed in some human cancers, yet its role in breast cancer remains unclear. Here, we report a functional analysis of RRS1 in breast cancer and its likely mechanism. Immunohistochemistry (IHC) and RT‐qPCR analyses indicated that RRS1 was commonly overexpressed in breast cancer tissues. The copy numbers of RRS1 were higher in tumours compared with those for normal tissues. And there was a significant correlation between copy number and mRNA expression. In addition, RRS1 overexpression was significantly correlated with lymph node metastasis and poor survival. RRS1 mRNA and protein levels were also significantly increased in a panel of human breast cancer cell lines. RRS1 knockdown inhibited proliferation and induced apoptosis and cell cycle arrest in all three cell lines. Furthermore, RRS1 knockdown suppressed the tumour formation and growth of MDA‐MB‐231 cells in nude mice. Additionally, RRS1 knockdown activated p53 and p21 in MCF‐7 cells. A marked increase in the quantity of ribosome‐free RPL11 was detected by Western blot. Moreover, co‐immunoprecipitation (CoIP) experiments showed that RRS1 knockdown activated p53 by facilitating the direct contact of MDM2 and RPL11/RPL5. Taken together, our results suggest that RRS1 may contribute to breast cancer proliferation through RPL11/MDM2‐mediated p53 activation. Therefore, RRS1 may be a promising target for breast cancer therapy.

Neuroblastoma (NB) is considered a highly prevalent extracranial solid tumor in young children, and the upregulation of N-myc proto-oncogene (MYCN) is closely associated with the late stages of NB and poor prognostic outcomes. The current study was designed to evaluate the effects of exosomal microRNA (miRNA/miR)-17-5p from MYCN-amplified NB cells on the proliferative and migratory potential of non-MYCN amplified NB cells. miR-17-5p was found to activate the PI3K/Akt signaling cascade by targeting PTEN, and the overexpression of miR-17-5p was found to promote cellular migration and proliferation in vitro . Further experimentation revealed that the elevated expression of miR-17-5p in SK-N-BE(2) cell-derived exosomes significantly promoted the proliferative and migratory capacities of SH-SY5Y cells by inhibiting PTEN. Collectively, these findings demonstrated that miR-17-5p derived from MYCN-amplified NB cell exosomes promoted the migration and proliferation of non-MYCN amplified cells, highlighting an exosome-associated malignant role for miR-17-5p.

Since malachite green was banned for using in food fish due to its carcinogenic and teratogenic effects on human, the search of alternative drug to treat Ichthyophthirius multifiliis becomes urgent. This study aimed to (1) evaluate the ethanol extracts of medicinal plants Cynanchum atratum, Zingiber officinale, Cynanchum paniculatum, immunostimulant (A), and immunostimulant (B) for their efficacy against I. multifiliis, and (2) determine effects of medicated feeds with C. atratum, Z. officinale, C. paniculatum, and immunostimulant (A) to treat I. multifiliis in grass carp. The results in this study showed that the minimum concentrations of C. atratum, Z. officinale, and C. paniculatum extracts for killing all theronts were 16, 8, and 16 mg/L, respectively. In vivo experiments, fish fed with medicated feeds of C. atratum for 10 days, or Z. officinale for 3 days, or combination of three plants for 10 days resulted in a significant reduction in the I. multifiliis infective intensity on grass carp after theronts exposure. Grass carp fed with medicated feeds of immunostimulant (A) for 21 days showed no infection and 100 % of survival 15 days post theronts exposure. Therefore, immunostimulant (A) is a promising feed supplement to treated I. multifiliis with good antiparasitic efficacy.

A regulator of ribosome synthesis 1 (RRS1) was discovered in yeast and is mainly localized in the nucleolus and endoplasmic reticulum. It regulates ribosomal protein, RNA biosynthesis, and protein secretion and is closely involved in cellular senescence, cell cycle regulation, transcription, translation, oncogenic transformation etc., Mutations in the RRS1 gene are associated with the occurrence and development of Huntington’s disease and cancer, and overexpression of RRS1 promotes tumor growth and metastasis. In this review, the structure, function, and mechanisms of RRS1 in various diseases are discussed.

The RRS1 regulator of ribosome synthesis has recently been reported a new target gene linked to cancer development. This study therefore investigates RRS1effectsb on BT549 cell proliferation and apoptosis in breast cancer. Western blot (WB) and real-time quantitative PCR (qPCR) were used to detect the relative expression of RRS1 in breast cancer cells BT-549 and the normal HMEC mammary gland epithelial cells. BT-549 cells were cultured and infected with retroviruses and RRS1 expression was detected by qPCR and WB. The MTT assay, Caspase-3/7 and flow cytometry (FCM) then detected growth and apoptosis in the BT549 breast cancer BT cell. WB detected the expression of Bcl-2 and Bax genes related to apoptosis at the protein level, and MTT assay confirmed that RRS1 knockdown significantly decreased cell viability (p<0.05) and induced apoptosis which was rescued by shRNA-RRS1 expression. The amount of caspase-3 increased significantly and apoptosis was obvious. The apoptotic cells amount analyzed by FCM was significantly increased and RRS1 knockdown also decreased the expression of apoptosis related protein bcl-2 and simultaneously increased the expression of Bax (p<0.05). Finally, the RRS1 gene was highly expressed in breast cancer cell line BT549 and its knockdown significantly reduced proliferation and apoptosis in BT549 cell. These results suggest that RRS1 is a novel gene related to breast cancer and has an important role in breast cancer proliferation and apoptosis.

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