The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/β-catenin signaling in cervical cancer.

Cervical cancer is one of the most common gynecological malignancies worldwide. Recently, the long noncoding RNAs (lncRNAs) have been shown to play essential roles in cervical cancer development and progression. This study investigated the role of lncRNA LINC00675 in cervical cancer and explored the relevant molecular mechanisms. LINC00675 expression was determined by quantitative real-time polymerase chain reaction; cell proliferation, migration and invasion were determined by Cell Counting Kit-8, Transwell migration, and invasion assays, respectively; cell apoptosis was measured by flow cytometry; protein levels were measured by western blot assay. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer. Overexpression of LINC00675 promoted cervical cancer cell proliferation, invasion, and migration. In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells. However, knockdown of LINC00675 played a contrasting role in cervical cancer cells. Overexpression of LINC00675 also increased the activity of Wnt/β-catenin signaling in cervical cancer cells, whereas knockdown of LINC00675 suppressed the activity of Wnt/β-catenin signaling. In addition, lithium chloride treatment attenuated the effects of LIC00675 knockdown on CaSki cell proliferation, invasion and migration. In vivo tumor growth study showed that knockdown of LINC00675 suppressed tumor growth, increased the protein levels of Bax and GSK-3β, and decreased the protein levels of Bcl-2 and β-catenin in isolated tumor tissues. In conclusion, our results implied that LINC00675 promoted cancer cell proliferation, migration, and invasion, and inhibit apoptosis likely by modulating the Wnt/β-catenin pathway.

Ma S ，Deng X ，Yang Y ，Zhang Q ，Zhou T ，Liu Z ... -  《-》

Downregulation of long noncoding RNA DGCR5 contributes to the proliferation, migration, and invasion of cervical cancer by activating Wnt signaling pathway.

Accumulating research works have reported that long noncoding RNAs (lncRNAs) are involved in various cancers, including cervical cancer. LncRNA DGCR5 has been identified in many cancers. However, the biological role of DGCR5 in cervical cancer remains barely known. We aimed to investigate the biological function of DGCR5 in cervical cancer progression. Here, in our current study, we observed that DGCR5 was downregulated in human cervical cancer cell lines (MS751, SiHa, HeLa, and HT-3) compared with the primary normal cervical squamous cells (NCSC1 and NCSC2). Then, DGCR5 was restrained by transfection with lenti-virus-short hairpin RNA (LV-shRNA) while induced by LV-DGCR5 in HeLa and C33A cells. Silence of DGCR5 obviously induced cervical cancer cell viability and cell proliferation. Reversely, upregulation of DGCR5 inhibited HeLa and C33A cell survival and proliferation. Furthermore, silencing of DGCR5 increased cervical cancer cell colony formation ability and decreased cell apoptosis, whereas its overexpression exhibited an opposite process. Moreover, DGCR5 suppressed migration and invasion capacity of cervical cancer cells. The Wnt signaling is integral in numerous biological processes. Here, we found that Wnt signaling was strongly activated in cervical cancer cells. Downregulation of DGCR5 contributed to cervical cancer progression by activating Wnt signaling. Subsequently, in vivo animal models were used to confirm that DGCR5 suppressed cervical cancer via targeting Wnt signaling. In conclusion, we reported that DGCR5 was involved in cervical cancer progression via modulating the Wnt pathway.

Liu Y ，Chang Y ，Lu S ，Xiang YY ... -  《-》

Long non-coding RNA LINC00675 inhibits tumorigenesis and EMT via repressing Wnt/β-catenin signaling in esophageal squamous cell carcinoma.

Zhong YB ，Shan AJ ，Lv W ，Wang J ，Xu JZ ... -  《-》

Highly expressed long non-coding RNA NNT-AS1 promotes cell proliferation and invasion through Wnt/β-catenin signaling pathway in cervical cancer.

Cervical cancer is the most common gynecological malignancies in women worldwide. The previous study showed that lncRNA NNT-AS1 could play an important role in tumor development and metastasis of colorectal cancer. However, little is known about the function of NNT-AS1 in cervical cancer. The aim of this study was to investigate the expression profile of NNT-AS1 in cervical cancer and assess its possible molecular mechanism. Relative expression levels of NNT-AS1 in cervical cancer tissues were determined by qRT-PCR. The biologic functions of NNT-AS1 in cervical cancer were explored by MTT assay, transwell assay and flow cytometric analysis in vitro. The influence of NNT-AS1 on tumorigenesis was measured by mice xenograft model. In addition, we evaluated the activation of Wnt/β-catenin signaling pathway by luciferase assay and western blot. Our results showed that NNT-AS1 expression in cervical cancer tissues compared with adjacent non-tumor tissues the overexpression of NNT-AS1 was positively associated with advanced FIGO stage, lymph node metastasis, depth of cervical invasion and poorer overall survival. Function assays showed that NNT-AS1 inhibition could suppress cervical cancer cells proliferation and invasion ability in vitro as well as the activation of Wnt/β-catenin signaling pathway. In vivo mice xenograft model revealed that silencing NNT-AS1 could reduce tumor growth in nude mice. The results of the current study suggested that NNT-AS1 might play an important role in cervical carcinogenesis and might serve as a potentially therapeutic target and prognostic marker in the treatment of cervical cancer.

Hua F ，Liu S ，Zhu L ，Ma N ，Jiang S ，Yang J ... -  《-》

Long noncoding RNA PCAT6 regulates cell growth and metastasis via Wnt/β-catenin pathway and is a prognosis marker in cervical cancer.

Lv XJ ，Tang Q ，Tu YQ ，Yan DD ，Wei QC ... -  《-》