Spindle assembly checkpoint (SAC) is a protective mechanism for cells to undergo accurate mitosis. SAC prevented chromosome segregation when kinetochores were not, or incorrectly attached to microtubules in the anaphase of mitosis, thus avoiding aneuploid chromosomes in daughter cells. Aneuploidy and altered expression of SAC component proteins are common in different cancers, including lung cancer. Therefore, SAC is a potential new target for lung cancer therapy. Five small molecule inhibitors of monopolar spindle 1 (MPS1), an upstream component protein of SAC, have entered clinical trials. This article introduces the biological functions of SAC, summarizes the abnormal expression of SAC component proteins in various cancers and the research progress of MPS1 inhibitors, and expects to provide a reference for the future development of lung cancer therapeutic strategies targeting SAC components.
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Humans ; Cell Cycle Proteins/metabolism* ; Spindle Apparatus/metabolism* ; Protein Serine-Threonine Kinases/metabolism* ; M Phase Cell Cycle Checkpoints/genetics* ; Lung Neoplasms/metabolism*

Angiomatoid Spitz nevus is a variant of melanocytic nevus with prominent vasculature. Due to its pathologic features, angiomatoid Spitz nevus in the vaginal wall is extremely rare. A 42-year-old woman presented to the hospital with abnormal vaginal bleeding. Vaginal examination revealed a 2×2-cm well-demarcated tumor on the posterior wall of the vagina. The mass was successfully removed by complete excision and was diagnosed as angiomatoid Spitz nevus on pathologic examination. We present the first reported case of vaginal angiomatoid Spitz nevus, which caused vaginal bleeding. Although angiomatoid Spitz nevus has many histopathological similarities with malignant melanoma, precise histopathological diagnosis is important for preventing overtreatment.
Adult ; Diagnosis ; Female ; Gynecological Examination ; Humans ; Medical Overuse ; Melanoma ; Nevus, Epithelioid and Spindle Cell ; Nevus, Pigmented ; Uterine Hemorrhage ; Vagina

To identify the component(s) involved in cell cycle control in the protozoan Giardia lamblia, cells arrested at the G1/S- or G2-phase by treatment with nocodazole and aphidicolin were prepared from the synchronized cell cultures. RNA-sequencing analysis of the 2 stages of Giardia cell cycle identified several cell cycle genes that were up-regulated at the G2-phase. Transcriptome analysis of cells in 2 distinct cell cycle stages of G. lamblia confirmed previously reported components of cell cycle (PcnA, cyclin B, and CDK) and identified additional cell cycle components (NEKs, Mad2, spindle pole protein, and CDC14A). This result indicates that the cell cycle machinery operates in this protozoan, one of the earliest diverging eukaryotic lineages.
Aphidicolin ; Cell Culture Techniques ; Cell Cycle ; Cell Cycle Checkpoints ; Cyclin B ; Gene Expression Profiling ; Genes, cdc ; Giardia lamblia ; Giardia ; Nocodazole ; Spindle Poles

No abstract available.
Nevus, Epithelioid and Spindle Cell*

Hyalinizing Spitz nevus was first introduced in 1994 by Suster. It is considered a rare variant in the spectrum of Spitz nevus, with only a dozen cases having been reported to date. Herein we report a case of a 28-year-old Korean woman who had a brown papular lesion on the left palm, which was diagnosed as hyalinizing Spitz nevus. Upon histopathological investigation, discohesive growth patterns of nevus cells in a hyalinized stroma were noted. Immunohistochemical stains showed positive reactivity of nevus cells with S-100 protein and vimentin, but negative stains with HMB-45 and CD68. This case demonstrates a rare variant of Spitz nevus located on an unusual site, and calls for awareness in the diagnosis of cutaneous lesions that histologically exhibit a prominent hyalinized stroma.
Adult ; Biopsy ; Coloring Agents ; Diagnosis ; Diagnosis, Differential ; Female ; Humans ; Hyalin* ; Nevus ; Nevus, Epithelioid and Spindle Cell* ; S100 Proteins ; Vimentin

Spitz nevus is a benign melanocytic nevus, common in children or young adults, and it has histological features that are confused with those of malignant melanoma. Polypoid Spitz nevus is the benign counterpart of polypoid malignant melanoma. A 22-year-old woman presented with a solitary 1.5×1.5 cm-sized firm polypoid erythematous nodule on the left thigh. On dermoscopy, pink to yellowish lagoons intermingled by white fibrous septa were found but milky red globules or irregular linear vessels were not found. Therefore, melanoma almost could be ruled out cautiously. Histopathology showed symmetrical, well-circumscribed, polypoid architecture with predominant dermal nests of spindle cells. Immunohistochemically, the nevus cells were strongly positive for S-100 protein and negative for HMB-45. Thus, the diagnosis of polypoid Spitz nevus was made. Herein, we report a case of polypoid Spitz nevus that was differentiated from polypoid melanoma by histopathologic and dermoscopic findings.
Child ; Dermoscopy ; Diagnosis ; Female ; Humans ; Melanoma ; Nevus ; Nevus, Epithelioid and Spindle Cell* ; Nevus, Pigmented ; S100 Proteins ; Thigh ; Young Adult

RSK2, also known as RPS6KA3 (ribosomal protein S6 kinase, 90 kDa, polypeptide 3), is a downstream kinase of the mitogen-activated protein kinase (MAPK) pathway, which is important in regulating survival, transcription, growth and proliferation. However, its biological role in mitotic progression is not well understood. In this study, we examined the potential involvement of RSK2 in the regulation of mitotic progression. Interestingly, depletion of RSK2, but not RSK1, caused the accumulation of mitotic cells. Time-lapse analysis revealed that mitotic duration, particularly the duration for metaphase-to-anaphase transition was prolonged in RSK2-depleted cells, suggesting activation of spindle assembly checkpoint (SAC). Indeed, more BubR1 (Bub1-related kinase) was present on metaphase plate kinetochores in RSK2-depleted cells, and depletion of BubR1 abolished the mitotic accumulation caused by RSK2 depletion, confirming BubR1-dependent SAC activation. Along with the shortening of inter-kinetochore distance, these data suggested that weakening of the tension across sister kinetochores by RSK2 depletion led to the activation of SAC. To test this, we analyzed the RSK2 effects on the stability of kinetochore–microtubule interactions, and found that RSK2-depleted cells formed less kinetochore–microtubule fibers. Moreover, RSK2 depletion resulted in the decrease of basal level of microtubule as well as an irregular distribution of mitotic spindles, which might lead to observed several mitotic progression defects such as increase in unaligned chromosomes, defects in chromosome congression and a decrease in pole-to-pole distance in these cells. Taken together, our data reveal that RSK2 affects mitotic progression by regulating the distribution, basal level and the stability of mitotic spindles.
Humans ; Kinetochores ; M Phase Cell Cycle Checkpoints ; Metaphase ; Microtubules ; Phosphotransferases ; Protein Kinases ; Ribosomal Protein S6 Kinases ; Ribosomal Protein S6 Kinases, 90-kDa* ; Siblings ; Spindle Apparatus*

No abstract available.
Nevus, Epithelioid and Spindle Cell*

No abstract available.
Child* ; Humans ; Nevus, Epithelioid and Spindle Cell*

BACKGROUND: Mutations in centrosomal protein genes have been identified in a number of genetic diseases in brain development, including microcephaly. Centrosomal P4.1-associated protein (CPAP) is one of the causal genes implicated in primary microcephaly. We previously proposed that CPAP is essential for mother centriole maturation during mitosis. METHODS: We immunostained CPAP-depleted cells using the ninein antibody, which selectively detects subdistal appendages in mature mother centrioles. RESULTS: Ninein signals were significantly impaired in CPAP-depleted cells. CONCLUSION: The results suggest that CPAP is required for mother centriole maturation in mammalian cells. The selective absence of centriolar appendages in young mother centrioles may be responsible for asymmetric spindle pole formation in CPAP-depleted cells.
Brain ; Cell Cycle ; Centrioles* ; Centrosome ; Humans ; Microcephaly ; Mitosis ; Mothers* ; Spindle Poles