Overexpression of CMTM7 inhibits cell growth and migration in liver cancer

Huang, Ziming; Li, Peng-ling; Yang, Peng; Hou, Xiaodan; Yang, Yili; Xu, Xin; Xu, Feng

doi:10.1002/kjm2.12058

Cited by 22 publications

(21 citation statements)

References 29 publications

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“…40 When liver cancer SK-Hep -1 cells were over-expressed with CMTM7, the expression of E-cadherin protein was increased and N-cadherin protein was decreased, indicating CMTM7 had a migration-suppressive ability. 41 The positive correlation between the expression of CMTM2 and E-cadherin in our study further confirms the role of CMTM members in cancer metastasis.…”

Section: Discussionsupporting

confidence: 82%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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Background: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated. Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay. Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P<0.05). Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.

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Section: Discussionsupporting

confidence: 82%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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“…In addition, another study has reported CMTM7 implicated in BCR expression and survival in B-1a cells [18]. Consistent with these studies, especially a recent study by Huang ZM et al, [19] CMTM7 exogenous expression in HCC cells signi cantly decreased cell proliferation and invasion, further con rmed the relationship between CMTM7 and tumor metastasis in HCC tissues.…”

Section: Discussionsupporting

confidence: 69%

Down-regulated CMTM7 promotes metastasis of hepatocellular carcinoma via its family member CMTM3

Zhu¹,

Bei²,

Di³

et al. 2020

Preprint

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Background Human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) members are found deregulated in various cancers and play a role in cancer development. Recent studies showed that CMTM7 was down-regulated in liver cancer and functioned as a tumor suppressor. Methods The expression of CMTM7 in hepatocellular carcinoma (HCC) tissues was measured by bioinformatics analysis, Western blot, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). CCK8 and cell colony formation assays were conducted to detect the cell proliferation. Cell invasion and migration ability was assessed by wound healing and Transwell assays. Results We identified a decreased expression of CMTM7 in HCC tissues was closely related to the metastasis and prognosis of HCC patients. To explore the effect of CMTM7 on the biological function of HCC cells, we over-expressed CMTM7 in two HCC cell lines, SK-Hep-1 and Bel-7402 cells. Cell proliferation was reduced significantly after exogenous expression of CMTM7, detected by both CCK8 and colony formation assay. Moreover, the invasion and migration ability of HCC cells were also inhibited by exogenous expression of CMTM7 in wound healing and Transwell assay. Furthermore, there was a significantly positive correlation between CMTM7 and CMTM3 both in HCC cells and tumor tissues. Conclusions Our results suggest that down-regulated CMTM7 promotes metastasis of HCC through inducing the expression of its family member CMTM3.

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“…Next, we show that negative expression of CMTM2 may participate in the progression of hepatocellular carcinoma. Several members, such as CMTM3, CMTM4, CMTM5 and CMTM7, have been documented to exhibit tumor suppressor functions in hepatocellular carcinoma cells [ 19 – 22 ]. In the present study, restoring CMTM2 expression not only inhibited liver cancer cell growth via G2/M phase accumulation without inducing apoptosis, but also suppressed cell metastasis and invasion in vitro.…”

Section: Discussionmentioning

confidence: 99%

Identification of Serum CMTM2 as a Potential Biomarker for HBV-Related Disorders

Chen

et al. 2020

Disease Markers

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Substantial advance supports that CMTM2 serve as an important performer in physiological and pathological processes. However, very little is clear about the relationship between CMTM2 and HBV-related disorders. Here, for the first time, we explore that whether or not serum CMTM2 is involved in HBV-related diseases. We found that CMTM2 values were significantly lower in patients compared to healthy control (p <0.001), using ELISA assay. Furthermore, serum CMTM2 levels were negatively correlated with HBV DNA levels in CHB patients but not correlated with the serum levels of ALT and AST. Serum CMTM2 concentrations were not correlated with the serum levels of ALT, AST and HBV DNA load in HBLC and HCC patients. In addition, analysis of the ROC curve indicated that CMTM2 levels were significantly associated with the diagnostic value of HBV-related disorders. Finally, downregulation of CMTM2 was observed in HBV-infected cell model. CMTM2 degradation could be attributed to HBx-activated Lys48 (K48)-linked polyubiquitination, which was abolished by treatment with the proteasome inhibitor MG132. HBV infection suppresses CMTM2 expression by activating ubiquitin-proteasome system. Serum CMTM2 levels can be adopted as an effective indicator of the pathogenesis of HBV-related disorders.

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Overexpression of CMTM7 inhibits cell growth and migration in liver cancer

Cited by 22 publications

References 29 publications

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Down-regulated CMTM7 promotes metastasis of hepatocellular carcinoma via its family member CMTM3

Identification of Serum CMTM2 as a Potential Biomarker for HBV-Related Disorders

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