ArticleBMC cancer2013
Targeting cell migration and the endoplasmic reticulum stress response with calmodulin antagonists: a clinically tested small molecule phenocopy of SEC62 gene silencing in human tumor cells.
Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 78 citations in OpenAlex.
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- Rules of Engagement for Components of Membrane Protein Biogenesis at the Human Endoplasmic Reticulum.International journal of molecular sciences · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
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- Quantitative Mass Spectrometry Characterizes Client Spectra of Components for Targeting of Membrane Proteins to and Their Insertion into the Membrane of the Human ER.International journal of molecular sciences · 2023Review
- The 3q OncogeneInternational journal of molecular sciences · 2023Article
- Repurposing the antipsychotic drug amisulpride for targeting synovial fibroblast activation in arthritis.JCI insight · 2023Article
- Sec61γ is a vital protein in the endoplasmic reticulum membrane promoting tumor metastasis and invasion in lung adenocarcinoma.British journal of cancer · 2023Article
- Editorial: The evolving picture of CaFrontiers in physiology · 2023Article
- Endoplasmic reticulum-resident protein Sec62 drives colorectal cancer metastasis via MAPK/ATF2/UCA1 axis.Cell proliferation · 2022Article
- ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum.Physiological reviews · 2022Review
- Sec62 promotes gastric cancer metastasis through mediating UPR-induced autophagy activation.Cellular and molecular life sciences : CMLS · 2022Article
- Effect of the 3q26-coding oncogeneFrontiers in physiology · 2022Article
- Sec61 complex/translocon: The role of an atypical ER CaFrontiers in physiology · 2022Review
- Signal Peptide Features Determining the Substrate Specificities of Targeting and Translocation Components in Human ER Protein Import.Frontiers in physiology · 2022Review
- Antagonizing Sec62 function in intracellular CaFrontiers in physiology · 2022Article
- The endoplasmic reticulum membrane protein Sec62 as potential therapeutic target inFrontiers in physiology · 2022Review
- Sec62 promotes pro-angiogenesis of hepatocellular carcinoma cells under hypoxia.Cell biochemistry and biophysics · 2021Article
- Development of a High-throughput NanoBRET Screening Platform to Identify Modulators of the RAS/RAF Interaction.Molecular cancer therapeutics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor cells benefit from their ability to avoid apoptosis and invade other tissues. The endoplasmic reticulum (ER) membrane protein Sec62 is a key player in these processes. Sec62 is essential for cell migration and protects tumor cells against thapsigargin-induced ER stress, which are both linked to cytosolic Ca²⁺. SEC62 silencing leads to elevated cytosolic Ca²⁺ and increased ER Ca²⁺ leakage after thapsigargin treatment. Sec62 protein levels are significantly increased in different tumors, including prostate, lung and thyroid cancer.
methodsIn lung cancer, the influence of Sec62 protein levels on patient survival was analyzed using the Kaplan-Meier method and log-rank test. To elucidate the underlying pathophysiological functions of Sec62, Ca²⁺ imaging techniques, real-time cell analysis and cell migration assays were performed. The effects of treatment with the calmodulin antagonists, trifluoperazine (TFP) and ophiobolin A, on cellular Ca²⁺ homeostasis, cell growth and cell migration were compared with the effects of siRNA-mediated Sec62 depletion or the expression of a mutated SEC62 variant in vitro. Using Biacore analysis we examined the Ca²⁺-sensitive interaction of Sec62 with the Sec61 complex.
resultsSec62 overproduction significantly correlated with reduced patient survival. Therefore, Sec62 is not only a predictive marker for this type of tumor, but also an interesting therapeutic target. The present study suggests a regulatory function for Sec62 in the major Ca²⁺ leakage channel in the ER, Sec61, by a direct and Ca²⁺-sensitive interaction. A Ca²⁺-binding motif in Sec62 is essential for its molecular function. Treatment of cells with calmodulin antagonists mimicked Sec62 depletion by inhibiting cell migration and rendering the cells sensitive to thapsigargin treatment.
conclusionsTargeting tumors that overproduce Sec62 with calmodulin antagonists in combination with targeted thapsigargin analogues may offer novel personalized therapeutic options.
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