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Recent Research Progress
C14orf166 is a 28 kD protein whose conserved gene is located on chromosome 14 at 14q22.1 and a transcriptional regulator associated with inhibition of centrosome structure. C14orf166 was originally identified as influenza A virus-associated gene; it promotes viral RNA replication and transcriptional activation by actively regulating host RNA polymerase (RNAP) II and viral RNAP activity. The interaction between C14orf166 and the viral polymerase complex is essential for this function. Besides, C14orf166 was reported to be a host protein that interacts with the hepatitis c virus during mRNA metabolism and affects host cell function. C14orf166 was also observed to regulate transcription and translation by interacting with various transactivators. It is thought to be a shuttling protein that transports RNAs between the nucleus and the cytoplasm and plays an important role in RNA fate and selective gene expression. C14orf166 has also been shown to be a binding partner of Janus kinase 2 (JAK2), which activates excessive signal transducer and activator of transcription 3 (STAT3) function to unbalancing its tumor promotion and anti-tumor function, thereby initiating tumor genesis. A growing number of studies have demonstrated that overexpression of C14orf166 has been identified in multiple malignant tumor tissues (including breast cancer, cervical carcinoma, bladder cancer and esophageal squamous cell carcinoma) compared to the adjacent, non-cancerous tissues in which they are paired.
C14orf166 is an unfavorable prognostic factor for breast cancer (BC) patients
BC is one of the leading causes of cancer deaths among women worldwide. Some drugs have been used to treat BC, but BC has developed resistance to some drugs. Prevention and treatment are important for BC, so finding new prognostic factors and BC targets is critical. Recent findings suggest that C14orf166 may be a novel prognostic biomarker of BC. The centrosome protein ninein interacts with glycogen synthase kinase 3beta (GSK-3β), and is phosphorylated by GSK-3β. The activity of JAK2 is inhibited by ninein, and the constitutive activation of JAK2 / STAT5 promotes resistance to apoptosis and promotes the occurrence of BC, which indicates that ninein may inhibit the development and progress of BC. C14orf166 interacts with ninein to block the phosphorylation of ninein catalyzed by GSK-3β, suggesting that C14orf166 may inhibit ninein and activate JAK2 to promote BC progression, but this prediction remains to be confirmed. The regulatory mechanism of C14orf166 remains to be explored. JAK2/STAT3 promotes self-renewal of BC stem cells, and CD24-CD44+ is a marker for BC stem cells. Activation of the JAK2/STAT3 pathway preferentially promotes self-renewal of C24-CD44+ BC stem cells. It reveals that C14orf166 may promote self-renewal of BC stem cells.
High expression of C14orf166 has value for the poor prognosis of cervical carcinoma
Cervical cancer is the third most common malignancy among women worldwide. Viral infection, genetic susceptibility and environmental factors are associated with the cause of cervical cancer. The development of cervical lesions from cervical intraepithelial neoplasia (CIN) to cervical cancer is a complex process triggered by persistent infection of the high-risk type of human papillomavirus (HPV). Altered expression of various oncogenes and tumor suppressor genes has also been associated with cervical cancer. Recent studies have shown that overexpression of C14orf166 is observed not only in HPV-positive cervical cancer cell lines such as HeLa, SiHa and CasKi, but also in HPV-negative cervical cancer cell line C33A. Moreover, lymph node metastasis is an important cause of cervical cancer-related death. Noordhuis et al. found that the 5-year overall survival rate for patients with early stage cervical cancer without lymph node metastasis was 90%, compared with only 65% for patients with lymph node metastasis. They observed a significant association between C14orf166 and pelvic lymph node metastasis. Therefore, further study of the role of C14orf166 in invasion and metastasis may help elucidate the mechanisms that regulate metastasis and identify new therapeutic targets for cervical cancer.
C14orf166 promotes proliferation of bladder cancer cells
Bladder cancer is a common genitourinary tumor worldwide. Mingkun Chen et al. found that C14orf166 was up-regulated in bladder cancer cells and tissues compared to normal bladder cells and tissues. C14orf166 promotes cell proliferation by regulating key regulatory proteins of G1 progression. Destructive cell cycle control is one of the leading causes of cancer development, where individuals with aberrant expression of cell cycle control genes have increased risk for bladder cancer. C14orf166 regulates cell cycle checkpoint proteins, suggesting that it may be a key regulator of bladder cancer progression. C14orf166 is associated with clinical features such as tumor size and survival time, and high expression of C14orf166 predicts poor prognosis and low survival. These results indicate that C14orf166 can be used not only as an oncogene, but also as a novel prognostic biomarker for patients with bladder cancer.
C14orf166 is associated with the occurrence and prognosis of esophageal squamous cell carcinoma (ESCC)
Esophageal cancer is one of the most common types of cancer in the world. ESCC is the main pathological type. Some scholars have detected the expression of C14orf166 in ESCC tissues, adjacent non-cancerous tissues and several esophageal cancer cell lines. The association between C14orf166 expression and the clinicopathological characteristics of ESCC were analyzed, highlighting the relationship between C14orf166 overexpression and ESCC occurrence, development and prognosis. Chen et al. reported that C14orf166, together with acyl glycerol kinase, were identified as JH2-interacting proteins that continuously activates the JAK2/STAT3 signaling pathway to promote esophageal squamous cell production and enhance cancer stem cell populations. JAK2 inhibitors will block ESCC growth via the JAK/STAT3 pathway.
In conclusion, C14orf166 is overexpressed in many tumors, however, the role of C14orf166 in cancer development and progression remains largely unknown. Consequently, further research on C14orf166 is of great significance and value for the clinical diagnosis and treatment of related tumors.
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