CMTM6 promotes hepatocellular carcinoma progression through stabilizing β-catenin
Copyright © 2023 Elsevier B.V. All rights reserved..
CMTM6, a regulator of PD-L1 stability, has been implicated in the development of various cancers. However, the expression and role of CMTM6 in hepatocellular carcinoma (HCC) remains controversial. Our study revealed a negative correlation between CMTM6 expression and HCC prognosis through bioinformatics analysis and immunofluorescence staining. CMTM6 expression was also positively associated with alpha-fetoprotein (AFP) levels, supporting its potential as a prognostic marker for HCC. Using Cmtm6 knockout mice, we found that Cmtm6 deficiency inhibited HCC formation and cell proliferation in primary liver cancer models induced by DEN and DEN/CCl4. In HCC cell lines, CMTM6 promoted cell proliferation and interacted with β-catenin, stabilizing it by preventing ubiquitination. In conclusion, our study suggested that CMTM6 upregulation promotes HCC cell proliferation through the β-catenin pathway, making it a potential therapeutic target for HCC treatment.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:583 |
|---|---|
| Enthalten in: |
Cancer letters - 583(2024) vom: 28. Feb., Seite 216585 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Liu, Qiyao [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
β-catenin |
|---|
| Anmerkungen: |
Date Completed 12.02.2024 Date Revised 12.02.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.canlet.2023.216585 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM365922978 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM365922978 | ||
| 003 | DE-627 | ||
| 005 | 20240212232021.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231227s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.canlet.2023.216585 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1289.xml |
| 035 | |a (DE-627)NLM365922978 | ||
| 035 | |a (NLM)38101607 | ||
| 035 | |a (PII)S0304-3835(23)00536-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Liu, Qiyao |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a CMTM6 promotes hepatocellular carcinoma progression through stabilizing β-catenin |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 12.02.2024 | ||
| 500 | |a Date Revised 12.02.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 Elsevier B.V. All rights reserved. | ||
| 520 | |a CMTM6, a regulator of PD-L1 stability, has been implicated in the development of various cancers. However, the expression and role of CMTM6 in hepatocellular carcinoma (HCC) remains controversial. Our study revealed a negative correlation between CMTM6 expression and HCC prognosis through bioinformatics analysis and immunofluorescence staining. CMTM6 expression was also positively associated with alpha-fetoprotein (AFP) levels, supporting its potential as a prognostic marker for HCC. Using Cmtm6 knockout mice, we found that Cmtm6 deficiency inhibited HCC formation and cell proliferation in primary liver cancer models induced by DEN and DEN/CCl4. In HCC cell lines, CMTM6 promoted cell proliferation and interacted with β-catenin, stabilizing it by preventing ubiquitination. In conclusion, our study suggested that CMTM6 upregulation promotes HCC cell proliferation through the β-catenin pathway, making it a potential therapeutic target for HCC treatment | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CMTM6 | |
| 650 | 4 | |a Hepatocellular carcinoma | |
| 650 | 4 | |a Proliferation | |
| 650 | 4 | |a Ubiquitination | |
| 650 | 4 | |a β-catenin | |
| 650 | 7 | |a beta Catenin |2 NLM | |
| 650 | 7 | |a Cmtm6 protein, mouse |2 NLM | |
| 700 | 1 | |a Wang, Jiahui |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Zixia |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Hanxiao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Yifan |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Pingzhang |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Ting |e verfasserin |4 aut | |
| 700 | 1 | |a Lu, Wenping |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Fujun |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Wenling |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Cancer letters |d 1976 |g 583(2024) vom: 28. Feb., Seite 216585 |w (DE-627)NLM000147273 |x 1872-7980 |7 nnns |
| 773 | 1 | 8 | |g volume:583 |g year:2024 |g day:28 |g month:02 |g pages:216585 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.canlet.2023.216585 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 583 |j 2024 |b 28 |c 02 |h 216585 | ||