TRIM29 prevents hepatocellular carcinoma progression by inhibiting Wnt/&amp;beta;-catenin signaling pathway

Xu, Mingxing; Hu, Jingxiong; Zhou, Boxuan; Zhong, Yi; Lin, Nan; Xu, Rui‐hua

doi:10.1093/abbs/gmy151

Cited by 30 publications

(22 citation statements)

References 30 publications

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“…Further experiments suggested that TRIM29 was targeted by miR-34a-5p. Previous studies have documented that TRIM29 functions as a tumor suppressor in several types of cancer, including breast cancer and hepatocellular carcinoma ( 23 , 40 ). By contrast, TRIM29 appears to function as a tumor promoter in lung-related cancers, and accelerates the progression of lung cancer ( 41 – 43 ).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA TP73‑AS1 accelerates the progression and cisplatin resistance of non‑small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA‑34a‑5p

et al. 2020

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non-small cell lung cancer (nSclc) is a leading subtype of lung cancer, with high mortality rates. recently, long non-coding rnas (lncrnas) have been associated with nSclc. The present study aimed to examine the role of the TP73 antisense rna 1 (TP73-aS1) lncrna in nSclc. TP73-aS1 and microrna(mir)-34a-5p expression levels were measured using reverse transcription-quantitative Pcr (rT-qPcr) and chromogenic in situ hybridization (ciSH). cell proliferation, apoptosis, migration and invasion was determined using Cell Counting Kit-8 (CCK-8), flow cytometry, Transwell and Matrigel assays, respectively. The median inhibitory concentration (ic 50) value of cisplatin (cis-diamminedichloroplatinum; ddP) was assessed using a ccK-8 assay. The interaction between mir-34a-5p and TP73-aS1 or tripartite motif-containing 29 (TriM29) was predicted using microrna. org and Starbase, then verified using a dual-luciferase reporter assay. The expression of TRIM29 was quantified at the mRNA and protein level using rT-qPcr and western blot analysis, respectively. TP73-AS1 was significantly upregulated, while mir-34a-5p was downregulated in nSclc tissues and cells. Functionally, TP73-aS1 knockdown inhibited proliferation, migration, invasion and ddP resistance, whilst inducing apoptosis in NSCLC cells. miR-34a-5p was identified as a target for TP73-aS1, and its inhibition reversed the effects of TP73-aS1 knockdown on nSclc cells. in addition, TriM29 was targeted by mir-34a-5p, and its overexpression reversed the effects of mir-34a-5p. Moreover, TP73-aS1 acted as a molecular sponge for mir-34a-5p, increasing the expression of TriM29. in conclusion, TP73-aS1 contributed to proliferation, migration and ddP resistance but inhibited apoptosis of nSclc cells by upregulating TriM29 and sponging mir-34a-5p.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA TP73‑AS1 accelerates the progression and cisplatin resistance of non‑small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA‑34a‑5p

et al. 2020

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“…47 TRIM29 can inhibit or activate the progression of hepatocellular carcinoma and colorectal cancer by targeting Wnt/β-catenin signaling pathway. 17 As a comprehensive bioinformatics analysis study, this article had some limitations. First, the possible mechanism of action for TRIM27 and related pathways has not been verified in in vivo or in vitro molecular biology experiments.…”

Section: F I G U R Ementioning

confidence: 99%

“…[13][14][15][16] In signaling pathways such as NF-κB, TGF-β, and PI3K/Akt, the TRIM family mediates the cell stemness of tumors and their ability to self-renew through excessive activation or abnormal signals of these pathways. [17][18][19][20] Currently, some TRIM proteins have been reported to have prognostic value and abnormal expression in cancer. Nevertheless, there has been no reported association between the TRIM family and the prognosis and occurrence of melanoma.…”

Section: Introductionmentioning

confidence: 99%

Identification of key genes and pathways for melanoma in the TRIM family

2020

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Certain members of the TRIM family have been shown to have abnormal expression and prognostic value in cancer. However, in the development and progression of melanoma, the role of different TRIM family members remains unknown. To address this issue, this study used the Oncomine, UCSC, Human Protein Atlas, DAVID, and GEPIA databases to study the role of TRIMs in the prognosis of melanoma. Differential expression of TRIM2, TRIM7, TRIM8, TRIM18 (MID1), TRIM19 (PML), TRIM27, and TRIM29 may play an important role in the development of melanoma. The expression TRIM7 and TRIM29 appeared to be helpful in the identification of primary tumors and metastases. Survival analysis suggested that the expression of TRIM27 significantly affected the overall survival and disease‐free survival of melanoma, and its expression was confirmed by qRT‐PCR. Our results indicated that the expression level of TRIM27 might be a prognostic marker of melanoma.

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“…TRIM29 is often mentioned that it has been involved in the response to DNA damage through its regulation of p53 and potentially functioned as an oncogene that promotes tumor growth 35 , 36 . Several studies suggested that TRIM29 promoted progression of cervical cancer 18 , pancreatic cancer 19 , colorectal cancer 21 , gastric cancer 37 , and glioma 38 , while suppressed progression of hepatocellular carcinoma via Wnt/beta-catenin signaling pathway 22 . It also has been reported that TRIM29 promoted proliferation and survival of bladder cancer cells through NF-κB but inhibited TWIST1 and suppressed EMT in breast cancer 23 .…”

Section: Discussionmentioning

confidence: 99%

“…TRIM29 has been found to be upregulated and associated with tumor progression and poor prognosis in cervical cancer 18 , pancreatic cancer 19 , gastric cancer 20 , and colorectal cancer 21 . On the contrary, TRIM29 functions as a tumor suppressor in hepatocellular carcinoma 22 and breast cancer 23 . Despite TRIM29 plays both promotive and suppressive roles in different cancers, a previous study reported that TRIM29 was upregulated and correlated with poor prognosis in TC patients, and functions as a oncogene via P13K/AKT signaling pathway 24 , another study observed that TRIM29 regulated cell growth via LncRNA HOXA11-AS/miR-761/TRIM29 axis 25 .…”

Section: Introductionmentioning

confidence: 99%

TRIM29 inhibits miR-873-5P biogenesis via CYTOR to upregulate fibronectin 1 and promotes invasion of papillary thyroid cancer cells

Zhang

Wang

et al. 2020

Cell Death Dis

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Papillary thyroid cancer (PTC) is the most common endocrine tumor with an increasing incidence, has a strong propensity for neck lymph node metastasis. Limited treatment options are available for patients with advanced or recurrent metastatic disease, resulting in a poor prognosis. Tripartite motif protein 29 (TRIM29) is dysregulated in various cancer and functions as oncogene or tumor suppressor in discrete cancers. In this study, we found that both TRIM29 and fibronectin 1 (FN1) were upregulated with positive correlation in PTC tissues. Neither overexpression nor downregulation of TRIM29 altered the proliferation of PTC cells significantly. Overexpression of TRIM29 significantly promotes, while knockdown of TRIM29 significantly decreases migration and invasion by regulating FN1 expression in PTC cells. In terms of mechanism, we found that TRIM29 altered the stability of FN1 mRNA via regulation of miR-873-5p expression. The current study also demonstrated that long non-coding RNA (LncRNA) CYTOR suppressed maturation of miR-873-5p via interaction with premiR-873, and TRIM29 decreased miR-873-5p via upregulation of CYTOR. This study suggests that involvement of TRIM29 in migration and invasion in PTC cells may reveal potential metastatic mechanism of PTC and represent a novel therapeutic target and strategy.

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TRIM29 prevents hepatocellular carcinoma progression by inhibiting Wnt/β-catenin signaling pathway

Cited by 30 publications

References 30 publications

Long non‑coding RNA TP73‑AS1 accelerates the progression and cisplatin resistance of non‑small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA‑34a‑5p

Long non‑coding RNA TP73‑AS1 accelerates the progression and cisplatin resistance of non‑small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA‑34a‑5p

Identification of key genes and pathways for melanoma in the TRIM family

TRIM29 inhibits miR-873-5P biogenesis via CYTOR to upregulate fibronectin 1 and promotes invasion of papillary thyroid cancer cells

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