STMN2 mediates nuclear translocation of Smad2/3 and enhances TGFβ signaling by destabilizing microtubules to promote epithelial-mesenchymal transition in hepatocellular carcinoma

Zhong, Fang-Jing; Sun, Bo; Cao, Momo; Xu, Cong; Li, Yiming; Yang, Lian-Yue

doi:10.1016/j.canlet.2021.03.001

Cited by 15 publications

(20 citation statements)

References 55 publications

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“…Migration and invasion, frequently accompanied by the epithelial-mesenchymal transition (EMT), lead to poor survival and high mortality in HCC [32,33]. Therefore, cell motility was investigated.…”

Section: Hyperthermia Inhibits Hcc Migration and Metastasismentioning

confidence: 99%

PFP@PLGA/Cu12Sb4S13-mediated PTT ablates hepatocellular carcinoma by inhibiting the RAS/MAPK/MT-CO1 signaling pathway

et al. 2021

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Hepatocellular carcinoma (HCC) is one of the most malignant tumors in the world, and patients with HCC face a poor prognosis. The conventional therapeutic strategies for HCC have undergone a challenge-riddled evolution owing to side effects and unsatisfactory efficacy. Here, aiming to provide a new method of HCC elimination, we formulated a novel multifunctional nanocapsule (PFP@PLGA/Cu12Sb4S13, PPCu) with applications in contrast-enhanced ultrasound imaging (CEUS) and photothermal therapy (PTT). These PPCu were successfully constructed with an average diameter of 346 nm (polydispersity index, PDI = 0.276). The reinforced contrast ratio of these PPCu was determined by CEUS, revealing their promising applications in image-guided monitoring of HCC treatment. Furthermore, the excellent photoabsorption and biocompatibility indicated by organ H&E staining indicated that PPCu meet quality expectations for use as photothermal transduction agent (PTA). PPCu treatment at 50 °C and higher temperatures efficiently repressed the proliferation, induced the apoptosis and decreased the motility of HCC cells. These effects might have been results of RAS/MAPK/MT-CO1 signaling pathway inhibition. In summary, PPCu were constructed to integrate CEUS and PTT successfully into therapy, which can lead to HCC elimination through RAS/MAPK/MT-CO1 signaling pathway repression.

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Section: Hyperthermia Inhibits Hcc Migration and Metastasismentioning

confidence: 99%

PFP@PLGA/Cu12Sb4S13-mediated PTT ablates hepatocellular carcinoma by inhibiting the RAS/MAPK/MT-CO1 signaling pathway

et al. 2021

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“…We rst found that STMN2 was overexpressed in PC patients, which was positively associated with tumor size, T stage, lymph node metastasis and the poor survival of PC patients. STMN2 was also overexpressed in hepatocellular, neuroblastoma and ovarian cancer [11][12][13]. STMN2 overexpression was associated with advanced clinical characters and bad prognosis in hepatocellular cancer [11].…”

Section: Discussionmentioning

confidence: 94%

“…STMN2 was also overexpressed in hepatocellular, neuroblastoma and ovarian cancer [11][12][13]. STMN2 overexpression was associated with advanced clinical characters and bad prognosis in hepatocellular cancer [11]. Meanwhile, it was an independent unfavorable prognostic factor in ovarian cancer [13].…”

Section: Discussionmentioning

confidence: 96%

“…Conversely, the speci c activator (KY19382) of WNT/β-catenin signaling reversed STMN2 silencing-inhibited EMT and cell proliferation. Only one study reports the function of STMN2 in the malignant behavior of cancer that STMN2 promotes cell migration, invasion and metastasis in vitro and in hepatocellular cancer by triggers EMT [11]. Taken together, STMN2, act as an oncogene, promotes the development of cancers partially by triggers EMT.…”

Section: Discussionmentioning

confidence: 99%

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STMN2 overexpression promotes cell proliferation and EMT in pancreatic cancer mediated by WNT/β-catenin signaling

Shao

Wang

Zhang

et al. 2022

Preprint

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Background: STMN2, as a key regulator in microtubule disassembly and dynamics, has been recently reported to participate in cancer development. However, the corresponding role in pancreatic ductal adenocarcinoma (PC), to our knowledge has not been reported. Methods: We investigate the potential role of STMN2 in the development of PC in vitro and vivo. Results: Overexpression of STMN2 was prevalently observed in human PC tissues compared with that in paired pancreas (44/81,54.3% vs 15/81, 18.5%, P<0.01), which was positively with multiple advanced stage of PC patients (tumor size, T stage, lymph-node metastasis and the poor survival). Meanwhile, a close correlation between high STMN2 and cytoplasmic/nuclear β-catenin expression (P=0.007) was observed in PC tissues and cell lines. STMN2 overexpression induced EMT and cell proliferation in vitro, which stimulated EMT-like cellular morphology, cell motility and proliferation, and the change of EMT (Snail1, E-cad and Vimentin) and Cyclin D1 signaling. However, XAV939 inhibited STMN2 overexpression-enhanced EMT and proliferation. Conversely, KY19382 reversed STMN2 silencing- inhibited EMT and cell proliferation in vitro. In addition, STMN2 promoted subcutaneous tumor growth with the overexpression of EMT and Cyclin D1 signaling. Finally, activated STMN2 and β-catenin were co-localized in cytoplasm/nuclear in vitro. Conclusions: β-catenin/TCF-mediated the transcription of STMN2. STMN2 overexpression promotes aggressive clinical stage of PC patients and promotes EMT and cell proliferation in vitro and vivo mediated by WNT/β-catenin signaling.

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“…The key features of EMT include the decrease in adhesion between cells or cells and the matrix, and cellular polarity, which leads to migration and invasion [12][13][14]. During the EMT process, epithelial cells undergo significant cytoskeletal rearrangement and transform into a mesenchymal phenotype with a fusiform cell shape and an increased ability for migration and invasion [15][16][17]. In addition, the expression of E-cadherin in cancer cells decreases [18], while the expression of N-cadherin and vimentin increases [19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway

Han

Meng

et al. 2021

IJMS

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Although some breast cancer patients die due to tumor metastasis rather than from the primary tumor, the molecular mechanism of metastasis remains unclear. Therefore, it is necessary to inhibit breast cancer metastasis during cancer treatment. In this case, after designing and synthesizing CTI-2, we found that CTI-2 treatment significantly reduced breast cancer cell metastasis in vivo and in vitro. Notably, with the treatment of CTI-2 in breast cancer cells, the expression level of E-cadherin increased, while the expression level of N-cadherin and vimentin decreased. In addition, after CTI-2 treatment, those outflow levels for p-ERK, p-p38, and p-JNK diminished, while no significant changes in the expression levels of ERK, JNK, or p38 were observed. Our conclusion suggested that CTI-2 inhibits the epithelial-mesenchymal transition (EMT) of breast carcinoma cells by inhibiting the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, thereby inhibiting the metastasis of breast tumor cells. Therefore, we believe that CTI-2 is another candidate for breast tumor medication.

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STMN2 mediates nuclear translocation of Smad2/3 and enhances TGFβ signaling by destabilizing microtubules to promote epithelial-mesenchymal transition in hepatocellular carcinoma

Cited by 15 publications

References 55 publications

PFP@PLGA/Cu12Sb4S13-mediated PTT ablates hepatocellular carcinoma by inhibiting the RAS/MAPK/MT-CO1 signaling pathway

PFP@PLGA/Cu12Sb4S13-mediated PTT ablates hepatocellular carcinoma by inhibiting the RAS/MAPK/MT-CO1 signaling pathway

STMN2 overexpression promotes cell proliferation and EMT in pancreatic cancer mediated by WNT/β-catenin signaling

CTI-2 Inhibits Metastasis and Epithelial-Mesenchymal Transition of Breast Cancer Cells by Modulating MAPK Signaling Pathway

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