Oral Oncology xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology
Letter to the Editor MicroRNA-138: A potential therapeutic target for head and neck squamous cell carcinoma (HNSCC)
We read with great interest the article by Islam et al. [1] published in Oral Oncology identifying that microRNA-138(miR-138) can downregulate RhoC via the direct targeting of its downstream molecules FAK, Src and Erk1/2 signaling pathway and subsequently result in cancer progression and survival. Recently, study revealed that deregulation of miR-138 was observed in three highly invasive HNSCC cell lines (UM1, 1386Ln and 686Ln) by examining the differential expression of microRNAs in six paired HNSCC cell lines with different metastatic potential (UM1/UM2, 1386Tu/ 1386Ln and 686Tu/686Ln) [2]. These findings indicated that miR138 may play a vital role in mediating HNSCC progression and prognosis and may be a potential therapeutic target for HNSCC. To date, HNSCC is an aggressive life-threatening disease related to high mortality rates. Many researches have been carried out to explore the molecular mechanisms that contribute to the initiation and progression of HNSCC. It was reported that VIM, ZEB2 and EZH2 were associated with epithelial–mesenchymal transition (EMT). Liu et al. [3] profiled that miR-138 can suppress EMT through the direct targeting of VIM, ZEB2 and EZH2 in HNSCC cell lines. As a result, it modulated HNSCC progression. Typically, miR138 was downregulated in HNSCC. An apparent inverted correlation between miR-138 and the levels of FOSL1 was observed in HNSCC tissue samples, and FOSL1 was essential to proliferation, apoptosis, cell motility, invasion, and metastasis [4]. A similar impact was seen in tongue squamous cell carcinoma (TSCC) [5,6]. Reduced miR-138 levels were observed in 13 out of 15 TSCC tissue samples as opposed to the control samples (adjacent histologically normal tissue samples) from the same patients, indicating that miR-138 expression was also frequently downregulated in TSCC. This in turn resulted in accentuated expression of GNAI2, which is a known proto-oncogene involved in the initiation and progression of tumors [6]. In addition, miR-138 could alter the expression
http://dx.doi.org/10.1016/j.oraloncology.2014.03.014 1368-8375/Ó 2014 Elsevier Ltd. All rights reserved.
of RhoC and ROCK2 and thereby contribute to tumour cell migration and invasion [5]. Collectively, available evidence suggests a pivotal role that miR138 plays in HNSCC. However, further studies are still needed to comprehensively explore the role of miR-138 in HNSCC. So, therapeutic agent targeting may lead to innovative new therapies for HNSCC. References [1] Islam M, Datta J, Lang JC, Teknos TN. Down regulation of RhoC by microRNA138 results in de-activation of FAK, Src and Erk signaling pathway in head and neck squamous cell carcinoma. Oral Oncol 2014. http://dx.doi.org/10.1016/ j.oraloncology.2014.01.014. [2] Liu X, Jiang L, Wang A, Yu J, Shi F, Zhou X. MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines. Cancer Lett 2009;286(2):217–22. [3] Liu X, Wang C, Chen Z, Jin Y, Wang Y, Kolokythas A, et al. MicroRNA-138 suppresses epithelial-mesenchymal transition in squamous cell carcinoma cell lines. Biochem J 2011;440(1):23–31. [4] Jin Y, Wang C, Liu X, Mu W, Chen Z, Yu D, et al. Molecular characterization of the microRNA-138-Fos-like antigen 1 (FOSL1) regulatory module in squamous cell carcinoma. J Biol Chem 2011;286(46):40104–9. [5] Jiang L, Liu X, Kolokythas A, Yu J, Wang A, Heidbreder CE, et al. Downregulation of the Rho GTPase signaling pathway is involved in the microRNA-138mediated inhibition of cell migration and invasion in tongue squamous cell carcinoma. Int J Cancer 2010;127(3):505–12. [6] Jiang L, Dai Y, Liu X, Wang C, Wang A, Chen Z, et al. Identification and experimental validation of G protein alpha inhibiting activity polypeptide 2 (GNAI2) as a microRNA-138 target in tongue squamous cell carcinoma. Hum Genet 2011;129(2):189–97.
Ji-Liang Xu Rong Xia Department of Stomatology, The Second Hospital of Anhui Medical University, Hefei, China E-mail addresses: [email protected] (J.-L. Xu), [email protected] (R. Xia) Available online xxxx
Contents lists available at ScienceDirect
Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology
Letter to the Editor MicroRNA-138: A potential therapeutic target for head and neck squamous cell carcinoma (HNSCC)
We read with great interest the article by Islam et al. [1] published in Oral Oncology identifying that microRNA-138(miR-138) can downregulate RhoC via the direct targeting of its downstream molecules FAK, Src and Erk1/2 signaling pathway and subsequently result in cancer progression and survival. Recently, study revealed that deregulation of miR-138 was observed in three highly invasive HNSCC cell lines (UM1, 1386Ln and 686Ln) by examining the differential expression of microRNAs in six paired HNSCC cell lines with different metastatic potential (UM1/UM2, 1386Tu/ 1386Ln and 686Tu/686Ln) [2]. These findings indicated that miR138 may play a vital role in mediating HNSCC progression and prognosis and may be a potential therapeutic target for HNSCC. To date, HNSCC is an aggressive life-threatening disease related to high mortality rates. Many researches have been carried out to explore the molecular mechanisms that contribute to the initiation and progression of HNSCC. It was reported that VIM, ZEB2 and EZH2 were associated with epithelial–mesenchymal transition (EMT). Liu et al. [3] profiled that miR-138 can suppress EMT through the direct targeting of VIM, ZEB2 and EZH2 in HNSCC cell lines. As a result, it modulated HNSCC progression. Typically, miR138 was downregulated in HNSCC. An apparent inverted correlation between miR-138 and the levels of FOSL1 was observed in HNSCC tissue samples, and FOSL1 was essential to proliferation, apoptosis, cell motility, invasion, and metastasis [4]. A similar impact was seen in tongue squamous cell carcinoma (TSCC) [5,6]. Reduced miR-138 levels were observed in 13 out of 15 TSCC tissue samples as opposed to the control samples (adjacent histologically normal tissue samples) from the same patients, indicating that miR-138 expression was also frequently downregulated in TSCC. This in turn resulted in accentuated expression of GNAI2, which is a known proto-oncogene involved in the initiation and progression of tumors [6]. In addition, miR-138 could alter the expression
http://dx.doi.org/10.1016/j.oraloncology.2014.03.014 1368-8375/Ó 2014 Elsevier Ltd. All rights reserved.
of RhoC and ROCK2 and thereby contribute to tumour cell migration and invasion [5]. Collectively, available evidence suggests a pivotal role that miR138 plays in HNSCC. However, further studies are still needed to comprehensively explore the role of miR-138 in HNSCC. So, therapeutic agent targeting may lead to innovative new therapies for HNSCC. References [1] Islam M, Datta J, Lang JC, Teknos TN. Down regulation of RhoC by microRNA138 results in de-activation of FAK, Src and Erk signaling pathway in head and neck squamous cell carcinoma. Oral Oncol 2014. http://dx.doi.org/10.1016/ j.oraloncology.2014.01.014. [2] Liu X, Jiang L, Wang A, Yu J, Shi F, Zhou X. MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines. Cancer Lett 2009;286(2):217–22. [3] Liu X, Wang C, Chen Z, Jin Y, Wang Y, Kolokythas A, et al. MicroRNA-138 suppresses epithelial-mesenchymal transition in squamous cell carcinoma cell lines. Biochem J 2011;440(1):23–31. [4] Jin Y, Wang C, Liu X, Mu W, Chen Z, Yu D, et al. Molecular characterization of the microRNA-138-Fos-like antigen 1 (FOSL1) regulatory module in squamous cell carcinoma. J Biol Chem 2011;286(46):40104–9. [5] Jiang L, Liu X, Kolokythas A, Yu J, Wang A, Heidbreder CE, et al. Downregulation of the Rho GTPase signaling pathway is involved in the microRNA-138mediated inhibition of cell migration and invasion in tongue squamous cell carcinoma. Int J Cancer 2010;127(3):505–12. [6] Jiang L, Dai Y, Liu X, Wang C, Wang A, Chen Z, et al. Identification and experimental validation of G protein alpha inhibiting activity polypeptide 2 (GNAI2) as a microRNA-138 target in tongue squamous cell carcinoma. Hum Genet 2011;129(2):189–97.
Ji-Liang Xu Rong Xia Department of Stomatology, The Second Hospital of Anhui Medical University, Hefei, China E-mail addresses: [email protected] (J.-L. Xu), [email protected] (R. Xia) Available online xxxx
