RNA interference knockdown of insulin receptor inhibits ovarian development in Chilo suppressalis.

BACKGROUND: The nutritional signaling pathway regulates an insect's size, development, and lifespan, as well as playing a vital role in reproduction. The insulin/insulin-like growth factor signaling (IIS) pathway plays a key role in the nutrition signaling pathway. As an integral component of the IIS pathway, insulin receptor (InR), a receptor tyrosine kinase, plays a role in the insulin pathway by controlling reproduction in many insect species. However, the precise molecular function of InR in non-model insect reproduction is poorly understood. METHODS: In our study, Chilo suppressalis, a well-known rice pest, was used as a molecular system to determine the role of InR in insect reproduction. Sequencing the InR gene of C. suppressalis, comparing the amino acid sequence-specific structure, and constructing a phylogenetic tree revealed that this gene has four main domains: ligand binding L domain, Furin-like region, fibronectin type III domains, and Tyrosine kinase catalytic domain, which were all highly conserved in insects. RESULTS: By characterizing the spatiotemporal expression profile of InR in different developmental stages and tissues, we found that InR gene expression was highest on the 3-day old in female pupae, 6th instar larvae, and fat body on the 6-day old in female pupae. InR gene expression may promote the molting and pupation of larvae and play a role in reproduction in the fat body. Furthermore, the RNA interference knockdown of InR dramatically reduced yolk deposition and blocked oocyte maturation. After suppression of InR, the expression of several other genes fluctuated to varying degrees. CONCLUSION: In conclusion, InR is vital to reproduction and is expected to become a new target for pest management.

MiR-139 prompts the development of osteosarcomas mainly through targeting ROCK1.

Abnormal expression of miR-139 was found to be aberrantly expressed in various tumors. However, whether it is involved in osteosarcomas (OS) has never been explored. In the current study, we found that the level of ROCK1 was markedly increased in OS cancer tissues compared to that of noncancerous tissues. Meanwhile, the expression of miR-139 was markedly reduced in OS cancer tissues and cell lines. Enhanced miR-139 expression markedly suppressed colony-formation and cell invasion capacity of OS cancer cells. Dual luciferase reporter assay demonstrated that ROCK1 was a target gene of miR-139. Moreover, overexpression of ROCK1 also led to increased invasion capacity in OS cancer cells even when miR-139 was inhibited, suggesting the anti-invasion effects of miR-139 were mediated through ROCK1. In summary, our present findings indicate that miR-139 functions as a tumor suppressor in OS cancer cells mainly by targeting ROCK1.