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c10orf99

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Official Full Name
chromosome 10 open reading frame 99
Synonyms
UNQ1833

Recent Research Progress

C10orf99 is a new type of human antimicrobial peptides (AMPS), which is also known as Ap-57. C10orf99 exhibited broad-spectrum antimicrobial activities against Gram-positive Staphylococcus aureus, Actinomyce, and Fungi Aspergillus niger as well as mycoplasma and lentivirus. C10orf99 has its distinct characteristics, including longer sequence length, four cysteines, highly cationic character, cellspecific toxicity, DNA binding and tissue-specific expressing patterns. Together, AP-57 is a new type of multifunctional AMPs worthy further investigation.

C10orf99, inhibits colon cancer cell growth through inducing G1 arrest

C10orf99 is a classical secreted protein with predicted molecular mass of 6.5 kDa, and a functional ligand of Sushi Domain Containing 2 (SUSD2). C10orf99 has the highest expression level in colon tissue. Both C10orf99 and SUSD2 are down-regulated in colon cancer tissues and cell lines with different regulation mechanisms. The expressional and functional characteristics of C10orf99 indicate it may be a tumor suppressor. Its gene is located on chromosome 10q23.1 beside the genomic region of tumor suppressor PTEN (10q23.3). Inactivation of tumor suppressor genes (TSGs) through promoter methylation, gene mutation, or loss of heterozygosity is important for carcinogenesis. In human colon cancer cell lines, the expression of C10orf99 cannot be restored by Aza or combined with trichostatin A (TSA), which indicates that it is not regulated by promoter methylation. The mechanism underlying the down-regulation of C10orf99 remains to be studied further.

Besides, C10orf99 has a contributive role in psoriasis pathogenesis and may be a new target for psoriasis treatment

Some studies have shown that the expressions of C10orf99 and its ortholog were significantly up-regulated in the skin of psoriasis patients and IMQ-induced psoriatic mouse models respectively. AKT, ERK1/2 and NF-κB signaling pathways play important roles in many biological functions. Studies have shown that the expression of all these protein kinases were significantly elevated in psoriatic skin and they play critical roles in the pathogenesis of psoriasis. The results of the study in vitro showed that M5 greatly activated the AKT, ERK1/2 and NF-κB signaling pathways. C10orf99 signaling was previously speculated to involve the AKT pathway. Knockdown of C10orf99 decreased the level of p-ERK1/2, but not p-AKT, in the cell culture model of psoriasis. In addition, C10orf99 knockdown resulted in a significant reduction of p-p65, indicative of the down-regulation of the NF-κB pathway activity. Conversely, over-expression of C10orf99 promoted the activity of ERK pathway and NF-κB pathway. Thus, C10orf99 likely regulates the proliferation of keratinocyte by activating the ERK1/2 and the NF-κB signaling. In summary, C10orf99 protein is highly expressed in psoriatic skin and it regulates keratinocyte proliferation likely through activation of the ERK1/2 and NF-κB pathway. Furthermore, down regulation of C10orf99 ameliorates IMQ-induced psoriasis in mice. Therefore, C10orf99 has a contributive role in psoriasis pathogenesis and may be a new target for psoriasis treatment.

In addition, the powerful anti-mycoplasma capacity of C10orf99 may provide new approach for mycoplasma therapy and prevention. It is worth carrying out further study to explore mechanisms underlying the cell specific effects of C10orf99, and the identification of C10orf99 as a distinct antimicrobial peptide will open up fruitful avenues of research.

References:

  1. Meijia Yang, et al. AP-57/C10orf99 is a new type of mutifunctional antimicrobial peptide. Biochemical and Biophysical Research Communications, 2015, 457: 347e352.
  2. Caifeng Chen, et al. C10orf99 contributes to the development of psoriasis by promoting the proliferation of keratinocytes. Scientific Reports, 2018, 8:8590.
  3. Wen Pan, et al. CSBF/C10orf99, a novel potential cytokine, inhibits colon cancer cell growth through inducing G1 arrest. Scientific Reports, 2014, 4:6812.
  4. Pi Guo, et al. Gene expression profile based classification models of psoriasis. Genomics, 2014, 103: 48–55.