Anti-INHBA monoclonal antibody, clone FQS3896(3)

Although it is well established that maturation conditions have a clear influence on oocyte developmental competence, it is not known whether this could be due to downstream effects of perturbation of the transcript profile of the oocyte's adjacent cumulus cells. Therefore, the aim of the present study was to compare the transcript profiles of cumulus cells derived from cumulus-oocyte complexes (COCs) matured in vitro or in vivo. Using a previously validated combined synchronisation and superstimulation protocol, COCs were recovered from beef heifer ovaries just before the expected time of the LH surge and matured in vitro, while in vivo-matured COCs were recovered just before ovulation (20 h after the LH surge). A custom-made cDNA microarray containing 2278 granulosa/cumulus transcripts was used for target and dye-swap hybridisations. In all, 64 genes were differentially expressed between the two groups. Transcript abundance of key genes associated with cumulus expansion (TNFAIP6) and regulation of oocyte maturation (INHBA and FST) were upregulated in in vivo-derived cumulus cells. However, cumulus cells derived from IVM COCs were enriched with genes involved in response to stress (HSPA5 and HSP90AB1). Quantitative real-time polymerase chain reaction confirmed the array results for eight of 10 genes selected for validation. The data presented here reveal that differences in oocyte developmental capacity after maturation in vitro or in vivo are accompanied by distinct differences in transcript abundance of the surrounding cumulus cells.

Inhibin, beta A (INHBA) is a member of the transforming growth factor (TGF-beta) family. The carcinogenic mechanisms of INHBA during the development of colorectal cancer (CRC) remain unclear. In the present study, we further elucidated the role of INHBA in CRC. We analysed the expression of INHBA in CRC and its relationship with patient prognosis using data from public databases. INHBA expression was evaluated in CRC tissues and cell lines using immunohistochemistry and western blotting. After inhibiting the expression of INHBA, the effect of INHBA on the function of CRC cells was evaluated in vitro. We found that INHBA was upregulated in CRC. High INHBA expression is closely related to poor prognosis in patients with CRC. Knockdown of INHBA in vitro can inhibit the proliferation, migration, and invasion of CRC cells. In terms of mechanism, we found that high INHBA expression activates the TGF-beta pathway. Significance of the study: INHBA acts as an oncogene in the progression of CRC and may, therefore, be a potential therapeutic target for CRC.