Cancer metastasis - tricks of the trade

Zeeshan, Rabia; Mutahir, Zeeshan

doi:10.17305/bjbms.2017.1908

Cited by 85 publications

(89 citation statements)

References 136 publications

(166 reference statements)

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“…23,24 Metastasis is also an important risk factor for cancer recurrence after clinical surgery, chemotherapy, or radiotherapy. 25,26 Because of high recurrence and high metastasis, HCC is one of the malignant tumors with the highest mortality rate. The identification of mechanism in HCC metastasis is in a need for HCC treatment and prognosis.…”

Section: Discussionmentioning

confidence: 99%

<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: Discussionmentioning

confidence: 99%

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

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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“…Therapeutics designed to address the prevention and progression of metastatic cancer are in demand. Metastatic cancers account for 90% of all cancer‐related deaths and are a leading cause of death worldwide . Survival at 5 years post diagnosis is 23%, representing a 76% decrease in survival compared to patients with nonmetastatic breast cancer .…”

Section: Receptors Targets For Inhibiting Metastasismentioning

confidence: 99%

Advances in Receptor‐Mediated, Tumor‐Targeted Drug Delivery

Large

Soucy

Hebert

et al. 2018

Advanced Therapeutics

141

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Receptor-mediated drug delivery presents an opportunity to enhance therapeutic efficiency by accumulating drug within the tissue of interest and reducing undesired, off-target effects. In cancer, receptor overexpression is a platform for binding and inhibiting pathways that shape biodistribution, toxicity, cell binding and uptake, and therapeutic function. This review will identify tumor-targeted drug delivery vehicles and receptors that show promise for clinical translation based on quantitative in vitro and in vivo data. The authors describe the rationale to engineer a targeted drug delivery vehicle based on the ligand, chemical conjugation method, and type of drug delivery vehicle. Recent advances in multivalent targeting and ligand organization on tumor accumulation are discussed. Revolutionizing receptor-mediated drug delivery may be leveraged in the therapeutic delivery of chemotherapy, gene editing tools, and epigenetic drugs.in the site of interest. This is clinically important as reaching a therapeutic dosage locally and reducing systemic toxicity can be life-threatening or life-saving events for cancer patients.The design of targeted DDVs can be optimized by altering the size, shape, material, ligand, and ligand orientation. For systemic delivery, spherical DDVs less than 200 nm in diameter are standard, which is balanced by the trade off between surface area and volume ratio. DDVs are prepared from biomaterials based on the size, hydrophobicity, and ideal release of the drug. There are a diverse range of ligand candidates for DDV functionalization, including monoclonal antibodies (mAbs), peptides, oligosaccharides, small molecules, and aptamers. [5] These ligands can be tethered to vehicles or conjugated directly to drugs by covalent (typically thiol or amide-based reactions, or "click" chemistry) or noncovalent attachment; the type of reaction is often based on the material of the DDV. [6] Multi-targeted and patterned DDVs improved cancer cell binding and the overall therapeutic benefit in vivo. The ideal DDV platform may be rationally designed by evaluating the drug, release mechanism, mode of delivery into the body, and target cells.Utilizing these approaches, targeted DDVs were successfully translated from the research setting into clinical use, or are currently in preclinical trials. [7] Liposomal based DDVs were approved for use in cancer therapy, treating fungal diseases, analgesics, photodynamic therapy, and viral vaccines. [8] Specifically, FDA approved liposomal drug formulations, such as Mepact, Maribo, and Epaxal were proven to be effective for the treatment of nonmetastatic osteosarcoma, acute lymphoblastic leukemia, and hepatitis A, respectively. [9] Many targeted DDVs in clinical use are utilized for the treatment of multiple cancer types, as there is often broad overlap in malignant receptor overexpression across various carcinogenic tissues (Figure 1). The widely successful drug Pembrolizumab (Keytruda), a humanized IgG4 isotype mAb that targets the programmed cell death (PD-1) rec...

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“…Distant metastasis is the end of a cancer patient. In cancer, cells could ow out of the primary loci by invading the surrounded vasculature or by lymphatic vessels [19][20][21]. It is published that tumor cells could secret matrix metal protease to melt the extracellular matrix and alter the permeability of blood vessels, which leads to leakage of blood vessels.…”

Section: Discussionmentioning

confidence: 99%

ANLN Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR Signaling Pathway

Wang

Zhang

et al. 2020

Preprint

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Background: Oral cancer is a malignant disease threatening human’s life and greatly reduces human’s life quality. ANLN was reported to promote progression in cancer. This study aims at investigating the role of ANLN and the molecular mechanism in oral cancer. Methods: ANLN was down-regulated by RNAi technology. The effect of ANLN on cell behaviors including proliferation, cycle distribution, invasion, and apoptosis was detected. Western blotting analysis was used to explore the mechanism of ANLN in oral cancer. Results: Based on data from TCGA database, ANLN was shown to be expressed significantly higher in tumor tissues than the normal control. Patients with higher ANLN expression exhibited shorter survival time. ANLN was also expressed abundantly in cancer cell lines CAL27 and HN30. When ANLN was knocked down in CAL27 and HN30 cells, cell proliferation and colony formation ability was downregulated. Cell invasion ability was also suppressed. But cell apoptosis rate was induced reversely. In addition, the level of critical members in PI3K signaling pathway including PI3K, mTOR, Akt, and PDK-1 were significantly reduced after ANLN was knocked down in CAL27 cells. Conclusions: ANLN contributes to progression in oral cancer and affects activation of PI3K/mTOR signaling pathway. This study provides a new potential target for therapy and drug development in oral cancer.

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Cancer metastasis - tricks of the trade

Cited by 85 publications

References 136 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>

Advances in Receptor‐Mediated, Tumor‐Targeted Drug Delivery

ANLN Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR Signaling Pathway

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Cancer metastasis - tricks of the trade

Cited by 85 publications

References 136 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>

Advances in Receptor‐Mediated, Tumor‐Targeted Drug Delivery

ANLN&nbsp;Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR&nbsp;Signaling Pathway

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ANLN Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR Signaling Pathway