SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma

Abstract

Recently, an increasing number of studies have reported that dysregulation of long noncoding RNAs (lncRNAs) plays an important role in cancer initiation and progression, including in epithelial ovarian carcinoma (EOC). However, little is known about the detailed biological functions of the lncRNA small nucleolar RNA host gene 22 (SNHG22) during the progression of EOC. Here, we found that SNHG22 was significantly increased in EOC tissues and was significantly associated with a low level of differentiation. Forced SNHG22 expression promoted chemotherapy resistance in EOC cells. Knockdown of SNHG22 expression increased the sensitivity of EOC cells to cisplatin and paclitaxel. Importantly, we found that SNHG22 could directly interact with miR-2467 and lead to the release of miR-2467-targeted Gal-1 mRNA. Moreover, SNHG22 overexpression induced EOC cell resistance to chemotherapy agents via PI3K/AKT and ERK cascade activation. In summary, our findings demonstrate that SNHG22 plays a critical role in the chemotherapy resistance of EOC by mediating the miR-2467/Gal-1 regulatory axis.

Long non-coding RNA SNHG22 facilitates the malignant phenotypes in triple-negative breast cancer via sponging miR-324-3p and upregulating SUDS3

“…In our work, SNHG22 was utilized to be our research object. In accordance with previous research, SNHG22 was proved to be highly expressed and could induce chemotherapy resistance through miR-2467/Gal-1 axis in epithelial ovarian carcinoma [13]. In our research, we detected abnormally strong expression of SNHG22 in TNBC tissues and cells.…”

“…Moreover, PVT1 was reported to facilitate malignant phenotypes of pancreatic cancer cells via absorbing miR-448 [12]. Small nucleolar RNA host gene 22 (SNHG22) is a novel lncRNA which was discovered as highly expressed and as a tumor-promoter in epithelial ovarian carcinoma cells through the miR-2467/ Gal-1 axis [13]. Nevertheless, the regulatory mechanism and function of SNHG22 in TNBC have not been elaborated.…”

<p>LINC01410 Knockdown Suppresses Cervical Cancer Growth and Invasion via Targeting miR-2467-3p/VOPP1 Axis</p>

“…7,8 LncRNA has been shown to exert various biological functions through diverse mechanisms, such as epigenetic regulation and microRNA sponging. 9,10 Increasing reports indicate that lncRNA regulates the development and progression of human cancers. [11][12][13] LncRNAs may regulate proliferation, invasiveness and differentiation of tumor cells.…”

LncRNA SNHG22 Sponges miR-128-3p to Promote Progression of Colorectal Cancer through Upregulating E2F3

“…20 Some researchers have reported the upregulated expression of SNHG22 in EOC, PTC, and ccRCC, and whose expression indicated poor prognosis in the three types of human malignancies. [11][12][13] In this study, we rst explored the expression patterns of SNHG22 in ANT, CRA, and CRC tissues, and found that SNHG22 expression was gradually upregulated in ANTs, CRA, and TTs. The high expression level of SNHG22 was associated with advanced T stage, node involvement, metastasis, and poor survival in CRC patients.…”

“…10 Several reports have found that SNHG22 contributed to cell growth, migration, invasion, and chemotherapy resistance in epithelial ovarian carcinoma (EOC), papillary thyroid cancer (PTC) and clear cell renal cell carcinoma (ccRCC). [11][12][13] Besides, upregulated SNHG22 was shown in TTs as compared with that in the ANTs, and whose high expression indicated poor prognosis in the three types of human malignancies. [11][12][13] To our knowledge, the biological role and expression patterns of SNHG22 have not been examined in human CRC.…”