Down‐regulated LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR‐212‐5p/FZD5/Wnt/β‐catenin axis

Peng, Naixiong; Zhang, Zejian; Wang, Yaomin; Yang, Minlong; Fan, Jiqing; Wang, Qinjun; Deng, Ling; Chen, Dong; Cai, Yuefeng; Li, Qihui; Wang, Xisheng; Li, Wei

doi:10.1111/jcmm.17000

Cited by 24 publications

(24 citation statements)

References 35 publications

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“…We found that GDPD4-2, AC144450.1, LINC01513, AC004009.2, AL096869.1, AP005210.1, and BX119924.1 were significantly underexpressed in PCa. LINC01513 was underexpressed in nasopharyngeal carcinoma (Wang J. et al, 2021). However, AC144450.1 has been found to be highly expressed in the breast tissue relative to the adjacent tissue (Hassani et al, 2021).…”

Section: Discussionmentioning

confidence: 95%

Astragalus–Scorpion Drug Pair Inhibits the Development of Prostate Cancer by Regulating GDPD4-2/PI3K/AKT/mTOR Pathway and Autophagy

You

et al. 2022

Front. Pharmacol.

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Objective: Prostate cancer (PCa) is an epithelial malignancy of the prostate that currently lacks effective treatment. Traditional Chinese medicine (TCM) can play an anticancer role through regulating the immune system, anti-tumor angiogenesis, regulating tumor cell apoptosis, autophagy dysfunction, and other mechanisms. This study attempted to explore the active ingredients and potential mechanism of action of the Astragalus–Scorpion (A–S) drug pair in PCa, in order to provide new insights into the treatment of PCa.Methods: Network pharmacology was used to analyze the A–S drug pair and PCa targets. Bioinformatics analysis was used to analyze the LncRNAs with significant differences in PCa. The expression of LC3 protein was detected by immunofluorescence. CCK8 was used to detect cell proliferation. The expressions of GDPD4-2, AC144450.1, LINC01513, AC004009.2, AL096869.1, AP005210.1, and BX119924.1 were detected by RT-qPCR. The expression of the PI3K/AKT/mTOR pathway and autophagy-related proteins were detected by western blot. LC-MS/MS was used to identify the active components of Astragalus and Scorpion.Results: A–S drug pair and PCa have a total of 163 targets, which were mainly related to the prostate cancer and PI3K/AKT pathways. A–S drug pair inhibited the formation of PCa, promoted the expression of LC3Ⅱ and Beclin1 proteins, and inhibited the expression of P62 and PI3K–AKT pathway proteins in PCa mice. Astragaloside IV and polypeptide extract from scorpion venom (PESV) were identified as the main active components of the A–S drug pair. GDPD4-2 was involved in the treatment of PCa by Astragaloside IV-PESV. Silencing GDPD4-2 reversed the therapeutic effects of Astragaloside IV-PESV by regulating the PI3K/AKT/mTOR pathway.Conclusion: Astragaloside IV-PESV is the main active components of A–S drug pair treated PCa by regulating the GDPD4-2/PI3K–AKT/mTOR pathway and autophagy.

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Section: Discussionmentioning

confidence: 95%

Astragalus–Scorpion Drug Pair Inhibits the Development of Prostate Cancer by Regulating GDPD4-2/PI3K/AKT/mTOR Pathway and Autophagy

You

et al. 2022

Front. Pharmacol.

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“…In cell lines increased expression of CARD8-AS1 reduces cell viability and affects cell migration and invasion abilities in lung adenocarcinoma cells by targeting miR-650. Accumulating evidence demonstrates the functional and clinical roles of lncRNAs involved in tumor progression [19][20][21]. For instance, lincRNA OIN1 is oncogenic in ovarian cancer and a potential molecular target for its treatment [22].…”

Section: Discussionmentioning

confidence: 99%

Identification of LncRNA CARD8-AS1 as a Potential Prognostic Biomarker Associated With Progression of Lung Adenocarcinoma

Zhang

2022

Br J Biomed Sci

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Introduction: Long non-coding RNAs (lncRNAs) exhibit crucial roles in human tumors. However, the role of lncRNA CARD8-AS1 in lung adenocarcinoma remains elusive. This study investigated the role of CARD8-AS1 in lung adenocarcinoma.Materials and Methods: The expression of CARD8-AS1 was detected by RT-qPCR analysis and confirmed using an online database. The clinical value of CARD8-AS1 was evaluated using the Kaplan-Meier curve and multivariate Cox regression analyses. The effects of CARD8-AS1 on cancer cell proliferation, migration, and invasion potential were assessed through several cellular experiments. Western blot assay was used to measure Bcl-2 and Bax protein levels. The interaction among CARD8-AS1, miR-650, and Bax, was assessed using a dual-luciferase reporter assay.Results: The expression of CARD8-AS1 was decreased in lung adenocarcinoma tissues and cell lines (p < 0.001). Low expression of CARD8-AS1 was related to tumor size (p = 0.042), TNM stage (p = 0.021), lymph node metastasis (p = 0.025), and poor overall survival (p < 0.05). Elevated expression of CARD8-AS1 could suppress cellular viability, migration potential, and invasion ability (p < 0.05). The Bcl-2 protein levels were decreased while Bax levels were increased by overexpression of CARD8-AS1 (p < 0.001). miR-650 may thus be a direct target of CARD8-AS1 and Bax may be a direct target of miR-650.Discussion: CARD8-AS1 expression was downregulated in lung adenocarcinoma and associated with several clinical parameters. CARD8-AS1 exerted tumor-suppressive effects by targeting the miR-650 and then regulating Bax expression. CARD8-AS1/miR-650 may serve as novel prognostic biomarkers and potential therapeutic targets for the treatment of lung adenocarcinoma.

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“…Transfected cells at the logarithmic growth stage were washed with a precooled PBS buffer, and 100 μ l of precooled RIPA (containing 1 μ L PMSF) was added. The cells were lysed on ice for 30 min, and the supernatant was collected by centrifugation and quantified by using the BCA protein quantification kit as described in the literature [ 17 ]. Samples were added to the gel wells at 70 μ g per lane and electrophoresed at a constant pressure of a 40 V (concentrate)/100 V (separator) until bromophenol reached the edge of the gel.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of LINC00936 Inhibits the Proliferation and Invasion of Endometrial Carcinoma Cells

Sun

2022

Journal of Oncology

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Objective. Endometrial carcinoma (EC) is one of the most common malignancies leading to death in women and poses a serious threat to women’s health. Therefore, exploring the molecular mechanisms affecting EC progression and metastasis is a clinical research hotspot. It has been shown that lncRNAs play an important role in the pathogenesis of EC. It is important to investigate the role of lncRNAs in the growth of EC to improve diagnosis and find new therapeutic targets of EC. Methods. The expression of LINC00936 in 36 EC tissues, paracancerous tissues, and cell lines was measured by fluorescence quantitative PCR. The relationship between LINC00936 expression and clinicopathological characteristics of patients was analyzed. The effects of overexpression of LINC00936 on proliferation, invasion, and migration of EC cells were examined by CCK-8 and transwell assays. Colony formation assay was also performed to evaluate the colony forming ability of EC cells. The effect of overexpression of LINC00936 on the expression of EMT-related proteins in EC cells was examined by western blot. In addition, the effect of LINC00936 overexpression on the growth of EC in vivo was examined by using tumorigenicity assay in the nude mouse. Results. LINC00936 was expressed at a low level in EC tissues and cell lines and significantly correlated with tumor size and lymphatic metastasis of patients. Overexpression of LINC00936 significantly inhibited the proliferation, invasion, and migration, as well as colony formation ability of EC cells. Western blot analysis showed that overexpression of LINC00936 significantly promoted the expression of E-cadherin and inhibited the expression of N-cadherin and vimentin in EC cells. Tumorigenic assays in the nude mouse demonstrated that overexpression of LINC00936 inhibited the growth of EC in vivo by suppressing Ki-67 and promoting E-cadherin expression. Conclusion. LINC00936 was expressed at a low level in EC tissues and significantly correlated with tumor size and lymphatic metastasis of patients. Overexpression of LINC00936 significantly inhibited the proliferation, invasion, and migration, as well as colony formation ability of EC cells. Therefore, LINC00936 could be a new target for the early diagnosis and treatment of EC patients.

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Down‐regulated LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR‐212‐5p/FZD5/Wnt/β‐catenin axis

Cited by 24 publications

References 35 publications

Astragalus–Scorpion Drug Pair Inhibits the Development of Prostate Cancer by Regulating GDPD4-2/PI3K/AKT/mTOR Pathway and Autophagy

Astragalus–Scorpion Drug Pair Inhibits the Development of Prostate Cancer by Regulating GDPD4-2/PI3K/AKT/mTOR Pathway and Autophagy

Identification of LncRNA CARD8-AS1 as a Potential Prognostic Biomarker Associated With Progression of Lung Adenocarcinoma

Overexpression of LINC00936 Inhibits the Proliferation and Invasion of Endometrial Carcinoma Cells

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