Sensory nerve niche regulates mesenchymal stem cell homeostasis via FGF/mTOR/autophagy axis.

Mesenchymal stem cells (MSCs) reside in microenvironments, referred to as niches, which provide structural support and molecular signals. Sensory nerves are niche components in the homeostasis of tissues such as skin, bone marrow and hematopoietic system. However, how the sensory nerve affects the behavior of MSCs remains largely unknown. Here we show that the sensory nerve is vital for mesenchymal tissue homeostasis and maintenance of MSCs in the continuously growing adult mouse incisor. Loss of sensory innervation leads to mesenchymal disorder and a decrease in MSCs. Mechanistically, FGF1 from the sensory nerve directly acts on MSCs by binding to FGFR1 and activates the mTOR/autophagy axis to sustain MSCs. Modulation of mTOR/autophagy restores the MSCs and rescues the mesenchymal tissue disorder of Fgfr1 mutant mice. Collectively, our study provides insights into the role of sensory nerves in the regulation of MSC homeostasis and the mechanism governing it.

The clinical manifestations, molecular mechanisms and treatment of craniosynostosis.

Craniosynostosis is a major congenital craniofacial disorder characterized by the premature fusion of cranial suture(s). Patients with severe craniosynostosis often have impairments in hearing, vision, intracranial pressure and/or neurocognitive functions. Craniosynostosis can result from mutations, chromosomal abnormalities or adverse environmental effects, and can occur in isolation or in association with numerous syndromes. To date, surgical correction remains the primary treatment for craniosynostosis, but it is associated with complications and with the potential for re-synostosis. There is, therefore, a strong unmet need for new therapies. Here, we provide a comprehensive review of our current understanding of craniosynostosis, including typical craniosynostosis types, their clinical manifestations, cranial suture development, and genetic and environmental causes. Based on studies from animal models, we present a framework for understanding the pathogenesis of craniosynostosis, with an emphasis on the loss of postnatal suture mesenchymal stem cells as an emerging disease-driving mechanism. We evaluate emerging treatment options and highlight the potential of mesenchymal stem cell-based suture regeneration as a therapeutic approach for craniosynostosis.

Optimized photochemistry enables efficient analysis of dynamic RNA structuromes and interactomes in genetic and infectious diseases.

Direct determination of RNA structures and interactions in living cells is critical for understanding their functions in normal physiology and disease states. Here, we present PARIS2, a dramatically improved method for RNA duplex determination in vivo with >4000-fold higher efficiency than previous methods. PARIS2 captures ribosome binding sites on mRNAs, reporting translation status on a transcriptome scale. Applying PARIS2 to the U8 snoRNA mutated in the neurological disorder LCC, we discover a network of dynamic RNA structures and interactions which are destabilized by patient mutations. We report the first whole genome structure of enterovirus D68, an RNA virus that causes polio-like symptoms, revealing highly dynamic conformations altered by antiviral drugs and different pathogenic strains. We also discover a replication-associated asymmetry on the (+) and (-) strands of the viral genome. This study establishes a powerful technology for efficient interrogation of the RNA structurome and interactome in human diseases.

Cranial Suture Regeneration Mitigates Skull and Neurocognitive Defects in Craniosynostosis.

Craniosynostosis results from premature fusion of the cranial suture(s), which contain mesenchymal stem cells (MSCs) that are crucial for calvarial expansion in coordination with brain growth. Infants with craniosynostosis have skull dysmorphology, increased intracranial pressure, and complications such as neurocognitive impairment that compromise quality of life. Animal models recapitulating these phenotypes are lacking, hampering development of urgently needed innovative therapies. Here, we show that Twist1+/- mice with craniosynostosis have increased intracranial pressure and neurocognitive behavioral abnormalities, recapitulating features of human Saethre-Chotzen syndrome. Using a biodegradable material combined with MSCs, we successfully regenerated a functional cranial suture that corrects skull deformity, normalizes intracranial pressure, and rescues neurocognitive behavior deficits. The regenerated suture creates a niche into which endogenous MSCs migrated, sustaining calvarial bone homeostasis and repair. MSC-based cranial suture regeneration offers a paradigm shift in treatment to reverse skull and neurocognitive abnormalities in this devastating disease.

Analyses of High-Risk Factors for Cervical Lymph Node Metastasis in Laryngeal Squamous Cell Carcinoma and Establishment of Nomogram Prediction Model.

Laryngeal squamous cell carcinoma (LSCC) is one of the most common laryngeal tumors, and its incidence is increasing yearly; however, whether lymph node dissection should be performed during surgery remains unclear. We retrospectively analyzed the clinical and pathological data of 246 cases of LSCC and developed a nomogram for the prediction of lymph node metastasis (LNM) of LSCC. The predictive performance and consistency of the model were evaluated using the consistency coefficient (C-index) and calibration curve, respectively. Among 246 cases of LSCC, 52 cases had metastasis with a positivity rate of 21.14%. Multivariate analyses showed that dysphagia, clinical T stage, and pathological differentiation were independent risk factors for LNM in LSCC. The accuracy of the contour map used to predict the risk for LNM was 0.809. Overall, this nomogram model can be used to evaluate LNM in patients with LSCC before surgery to decide whether to conduct neck dissection and improve patient prognosis.

C9orf72 and smcr8 mutant mice reveal MTORC1 activation due to impaired lysosomal degradation and exocytosis.

How lysosome and MTORC1 signaling interact remains elusive in terminally differentiated cells. A G4C2 repeat expansion in C9orf72 is the most common cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (C9ALS-FTD). We previously identified a C9orf72-SMCR8-containing complex. Here we found that c9orf72 and smcr8 double-knockout (dKO) mice exhibit similar but more severe immune defects than the individual knockouts. In c9orf72 or smcr8 mutant macrophages, lysosomal degradation and exocytosis were impaired due to the disruption of autolysosome acidification. As a result of impaired lysosomal degradation, MTOR protein was aberrantly increased, resulting in MTORC1 signaling overactivation. Inhibition of hyperactive MTORC1 partially rescued macrophage dysfunction, splenomegaly and lymphadenopathy in c9orf72 or smcr8 mutant mice. Pharmacological inhibition of lysosomal degradation upregulated MTOR protein and MTORC1 signaling in differentiated wild-type macrophages, which resemble phenotypes in KO mice. In contrast, C9orf72 or Smcr8 depletion in proliferating macrophages decreased MTORC1 signaling. Our studies causatively link C9orf72-SMCR8's cellular functions in lysosomal degradation, exocytosis, and MTORC1 signaling with their organism-level immune regulation, suggesting cell state (proliferation vs. differentiation)-dependent regulation of MTOR signaling via lysosomes.Abbreviations: ALS: amyotrophic lateral sclerosis; ATG13: autophagy related 13; BMDMs: bone marrow-derived macrophages; BafA1: bafilomycin A1; C9orf72: C9orf72, member of C9orf72-SMCR8 complex; CD68: CD68 antigen; ConA: concanamycin A; dKO: double knockout; DENN: differentially expressed in normal and neoplastic cells; FTD: frontotemporal dementia; GEF: guanine nucleotide exchange factor; IFNB1: interferon beta 1, fibroblast; IFNG: interferon gamma; IL1B/IL-1ß: interleukin 1 beta; IL6: interleukin 6; iPSCs: induced pluripotent stem cells; LAMP1: lysosomal-associated membrane protein 1; LPOs: LAMP1-positive organelles; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; LPS: lipopolysaccharide; MTORC1: mechanistic target of rapamycin kinase complex 1; MEFs: mouse embryonic fibroblasts; MNs: motor neurons; NOS2/iNOS: nitric oxide synthase 2, inducible; RAN: repeat-associated non-AUG; RB1CC1/FIP200: RB1-inducible coiled-coil 1; RPS6/S6: ribosomal protein S6; RPS6KB1/S6K1: ribosomal protein S6 kinase, polypeptide 1; SMCR8: Smith-Magenis syndrome chromosome region, candidate 8; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TNF: tumor necrosis factor; TSC1: TSC complex subunit 1; ULK1: unc-51 like kinase 1; v-ATPase: vacuolar-type H⁺-translocating ATPase.

Lin28-mediated temporal promotion of protein synthesis is crucial for neural progenitor cell maintenance and brain development in mice.

Neural progenitor cells (NPCs) undergo rapid proliferation during neurulation. This rapid growth generates a high demand for mRNA translation in a timing-dependent manner, but its underlying mechanism remains poorly understood. Lin28 is an RNA-binding protein with two paralogs, Lin28a and Lin28b, in mammals. Mice with Lin28b deletion exhibit no developmental defects, whereas we have previously reported that Lin28a deletion leads to microcephaly. Here, we find that Lin28a/b double knockout (dKO) mice display neural tube defects (NTDs) coupled with reduced proliferation and precocious differentiation of NPCs. Using ribosomal protein 24 hypomorphic mice (Rpl24Bst/+ ) as a genetic tool to dampen global protein synthesis, we found that Lin28a-/-;Rpl24Bst/+ compound mutants exhibited NTDs resembling those seen in Lin28a/b dKO mice. Increased NPC numbers and brain sizes in Lin28a-overexpressing mice were rescued by Rpl24Bst/+ heterozygosity. Mechanistically, polysome profiling revealed reduced translation of genes involved in the regulation of cell cycle, ribosome biogenesis and translation in dKO mutants. Ribosome biogenesis was reduced in dKO and increased in Lin28a-overexpressing NPCs. Therefore, Lin28-mediated promotion of protein synthesis is essential for NPC maintenance and early brain development.

Mesenchyme homeobox 1 mediates transforming growth factor-ß (TGF-ß)-induced smooth muscle cell differentiation from mouse mesenchymal progenitors.

Differentiation of smooth muscle cells (SMCs) is critical for proper vasculogenesis and angiogenesis. However, the molecular mechanisms controlling SMC differentiation are not completely understood. During embryogenesis, the transcription factor mesenchyme homeobox 1 (Meox1) is expressed in the early developing somite, which is one of the origins of SMCs. In the present study, we identified Meox1 as a positive regulator of SMC differentiation. We found that transforming growth factor-ß (TGF-ß) induces Meox1 expression in the initial phase of SMC differentiation of pluripotent murine C3H10T1/2 cells. shRNA-mediated Meox1 knockdown suppressed TGF-ß-induced expression of SMC early markers, whereas Meox1 overexpression increased expression of these markers. Mechanistically, Meox1 promoted SMAD family member 3 (Smad3) nuclear retention during the early stage of TGF-ß stimulation because Meox1 inhibited protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) and thereby prevented PPM1A-mediated Smad3 dephosphorylation. Meox1 appears to promote PPM1A degradation, leading to sustained Smad3 phosphorylation, thus allowing Smad3 to stimulate SMC gene transcription. In vivo, Meox1 knockdown in mouse embryos impaired SMC marker expression in the descending aorta of neonatal mice, indicating that Meox1 is essential for SMC differentiation during embryonic development. In summary, the transcriptional regulator Meox1 controls TGF-ß-induced SMC differentiation from mesenchymal progenitor cells by preventing PPM1A-mediated Smad3 dephosphorylation, thereby supporting SMC gene expression.

Brain cytoplasmic RNA 1 suppresses smooth muscle differentiation and vascular development in mice.

The cardiovascular system develops during the early stages of embryogenesis, and differentiation of smooth muscle cells (SMCs) is essential for that process. SMC differentiation is critically regulated by transforming growth factor (TGF)-ß/SMAD family member 3 (SMAD3) signaling, but other regulators may also play a role. For example, long noncoding RNAs (lncRNAs) regulate various cellular activities and events, such as proliferation, differentiation, and apoptosis. However, whether long noncoding RNAs also regulate SMC differentiation remains largely unknown. Here, using the murine cell line C3H10T1/2, we found that brain cytoplasmic RNA 1 (BC1) is an important regulator of SMC differentiation. BC1 overexpression suppressed, whereas BC1 knockdown promoted, TGF-ß-induced SMC differentiation, as indicated by altered cell morphology and expression of multiple SMC markers, including smooth muscle α-actin (αSMA), calponin, and smooth muscle 22α (SM22α). BC1 appeared to block SMAD3 activity and inhibit SMC marker gene transcription. Mechanistically, BC1 bound to SMAD3 via RNA SMAD-binding elements (rSBEs) and thus impeded TGF-ß-induced SMAD3 translocation to the nucleus. This prevented SMAD3 from binding to SBEs in SMC marker gene promoters, an essential event in SMC marker transcription. In vivo, BC1 overexpression in mouse embryos impaired vascular SMC differentiation, leading to structural defects in the artery wall, such as random breaks in the elastic lamina, abnormal collagen deposition on SM fibers, and disorganized extracellular matrix proteins in the media of the neonatal aorta. Our results suggest that BC1 is a suppressor of SMC differentiation during vascular development.

MiR-302/367 regulate neural progenitor proliferation, differentiation timing, and survival in neurulation.

How neural progenitor cell (NPC) behaviors are temporally controlled in early developing embryos remains undefined. The in vivo functions of microRNAs (miRNAs) in early mammalian development remain largely unknown. Mir-302/367 is a miRNA cluster that encodes miR-367 and four miR-302 members (miR302a-d). We show that miR-302b is highly expressed in early neuroepithelium and its expression decline as development progresses. We generated a mir-302/367 knockout mouse model and found that deletion of mir-302/367 results in an early embryonic lethality and open neural tube defect (NTD). NPCs exhibit enhanced proliferation, precocious differentiation, and decreased cell survival in mutant embryos. Furthermore, we identified Fgf15, Cyclin D1, and D2 as direct targets of miR-302 in NPCs in vivo, and their expression is enhanced in mutant NPCs. Ectopic expression of Cyclin D1 and D2 increases NPC proliferation, while FGF19 (human ortholog of Fgf15) overexpression leads to an increase of NPC differentiation. Thus, these findings reveal essential roles of miR-302/367 in orchestrating gene expression and NPC behaviors in neurulation; they also point to miRNAs as critical genetic components associated with neural tube formation.

Microcephaly disease gene Wdr62 regulates mitotic progression of embryonic neural stem cells and brain size.

Human genetic studies have established a link between a class of centrosome proteins and microcephaly. Current studies of microcephaly focus on defective centrosome/spindle orientation. Mutations in WDR62 are associated with microcephaly and other cortical abnormalities in humans. Here we create a mouse model of Wdr62 deficiency and find that the mice exhibit reduced brain size due to decreased neural progenitor cells (NPCs). Wdr62 depleted cells show spindle instability, spindle assembly checkpoint (SAC) activation, mitotic arrest and cell death. Mechanistically, Wdr62 associates and genetically interacts with Aurora A to regulate spindle formation, mitotic progression and brain size. Our results suggest that Wdr62 interacts with Aurora A to control mitotic progression, and loss of these interactions leads to mitotic delay and cell death of NPCs, which could be a potential cause of human microcephaly.

[Longterm impact on swallowing quality-of-life after partial laryngectomy].

OBJECTIVE: To discuss the longterm quality-of-life related to swallowing function after different partial laryngectomy. METHODS: The worldwide known swallow quality-of-life questionnaire (SWAL-QOL, Hongkong, Chinese edition); was used in this research to evaluate the swallowing QOL on 96 postoperative patients who underwent different kinds of partial laryngectomy more than one year before. The patients were divided into 4 groups: supracricoid partial laryngectomy-cricohyoidopexy (SCPL-CHP), supracricoid partial laryngectomy-cricohyoidoepiglottopexy (SCPL-CHEP), horizontal supraglottic partial laryngectomy (horizontal PL), and vertical partial laryngectomy (vertical PL). RESULTS: A one-way MANOVA revealed a significant multivariate (the 11 scales of SWAL-QOL) main effect for groups (P < 0.01), and significant univariate main effects were obtained for groups in 9 scales out of 11 (P < 0.01). In all the 9 scales vertical PL group acquired near full scores except the communication scale, and was significantly higher than the other 3 groups in many scales (P < 0.05). CHP group acquired the worst scores of the 4 groups, showing significant differences in most of the 9 scales (P < 0.05). No significant difference was found between Horizontal PL and CHEP except in communication (P > 0.05). Patients with deglutition disorders (choke/cough) had a lower score in the social function scale. CONCLUSIONS: Swallowing quality-of-life of postoperative patients was deeply influenced even when more than one year had passed after surgery. Some of them felt deeply burdened by deglutition disorder. Patients after CHP proved to have a worst quality of life than the others, while vertical PL the best. The QOL between Horizontal PL and CHEP was shown to be almost the same. The influence over QOL from longterm dysphagia was multi-dimensional, containing the degeneration of social function.

[Comparison of postoperative deglutition disorder in patients with laryngeal carcinoma after different types of supracricoid partial laryngectomy].

OBJECTIVE: To Evaluate the incidence rates and extents of deglutition disorder in patients with laryngeal carcinoma after different types of supracricoid partial laryngectomy. METHODS: Retrospective analysis of postoperative deglutition disorder in patients with laryngeal carcinoma after different types of supracricoid partial laryngectomy treated in our department from 2005 to 2009. The extents of postoperative deglutition disorder were evaluated using a homemade quantitative score table at 5-20 days postoperation. RESULTS: The score of deglutition disorder was 2.71 ± 0.31 in the supracricoid partial laryngectomy-cricohyoidoepiglottopexy (SCPL-CHEP) operation group and 3.43 ± 0.64 in the supracricoid partial laryngectomy-cricohyoidopexy (SCPL-CHP) group, respectively. The deference was statistically significant between the two groups (P < 0.001). The coefficient between age and score of postoperative deglutition disorder was assessed by Pearson correlation analysis. The coefficient of correlation was 0.947 (P < 0.0001) in the SCPL-CHEP group and 0.907 (P < 0.0001) in the SCPL-CHP group. The incidence rate of deglutition disorder was 1/37 in the SCPL-CHEP group and 7/30 in the SCPL-CHP group, evaluated at 8 weeks postoperation (P = 0.012). The deference between the two groups was significant. CONCLUSIONS: The type of operation procedure is an important factor affecting the occurrence of postoperative deglutition disorder in the patients after supracricoid partial laryngectomy, more serious in the SCPL-CHP group. The severity of postoperative deglutition disorder is more serious along with the increase of patient's age. For the elderly (> 70 years of age) patients with laryngeal carcinoma, the choice of surgical procedure should be more cautious, especially with the SCPL-CHP operation.

[Comparing extended vertical partial laryngectomy and cricohyoidoepiglottopexy in the treatment of laryngeal carcinoma].

OBJECTIVE: To compare the results of extended vertical partial laryngectomy (similar to modified supracricoid partial laryngectomy with cricohyoidoepiglottopexy) and cricohyoidoepiglottopexy in the treatment of laryngeal carcinoma. METHODS: Retrospectively analyzed on the results and prognosis in patients underwent extended vertical partial laryngectomy and cricohyoidoepiglottopexy between 1998 and 2005. The operation was similar to extended vertical partial laryngectomy. The healthy vocal cord and ventricular band as well as about 1/3 to 2/3 laminas of thyroid cartilage were removed. The healthy cricoarytenoid joint was reserved. The vocal cord, ventricular band, fixed or limitation of motion arytenoid cartilage and 2/3 laminas of thyroid cartilage in ill side were removed. The posteroinferior border of laminas of thyroid cartilage in both sides were reserved. The cricoid was lifted and fixed with hyoid epiglottis directly. Extended vertical partial laryngectomy group consisted of 37 patients with glottic carcinoma (stage T2 16 cases, stage T3 21 cases) and cricohyoidoepiglottopexy group consisted of 34 patients with glottic carcinoma (stage T2 12 cases, stage T3 21 cases, stage T4 1 case). RESULTS: Kaplan-Meier analysis was performed to calculate the survival rates. The three-year cumulative survival rate was 91.7% in extended vertical partial laryngectomy group and 87.5% in cricohyoidoepiglottopexy group respectively. There was no significant difference between the two groups (P > 0.05). The five-year cumulative survival rate was 80.6% in extended vertical partial laryngectomy group and 81.3% in cricohyoidoepiglottopexy group respectively. There was also no significant difference between the two groups (P > 0.05). The decannulation rate was 100% (37/37) in extended vertical partial laryngectomy group and 94.1% (32/34) in cricohyoidoepiglottopexy group respectively. The decannulation time was (14.0 + or - 2.3) days in extended vertical partial laryngectomy group and (19.0 + or - 4.6) days in cricohyoidoepiglottopexy group respectively. The incidence of aspiration was 2.7% (1/37) in modified group and 23.5 (8/34) in cricohyoidoepiglottopexy group respectively evaluated at 8th weeks post-operatively. The evaluation of deglutition disorder was analyzed by Ridit analysis in both groups and the results showed that there was significant difference between the two groups (U = 7.341, P < 0.001). The symptom of aspiration in extended vertical partial laryngectomy group was significant less than in cricohyoidoepiglottopexy group. CONCLUSIONS: Although the survival rate was not different between the two groups. The preservation of laryngeal function in extended vertical partial laryngectomy group was significant better than in cricohyoidoepiglottopexy group and extended vertical partial laryngectomy.

[Glottic measurement and vocal evaluation after three surgical techniques in the treatment of bilateral vocal cord paralysis].

OBJECTIVE: To evaluate postoperative glottic area and vocal quality of three various surgical techniques for treating bilateral vocal cord paralysis, including laser arytenoidectomy (Group A, 24 cases), reinnervation of the posterior cricoarytenoid muscle by phrenic nerve (Group B, 9 cases) and arytenoidectomy accompanying lateral cordopexy by extralaryngeal approach (Woodman's procedure, Group C, 13 cases). METHODS: 46 cases suffered from bilateral recurrent laryngeal nerve injury were included in our study. The pre-postoperative glottic measurement and vocal acoustic parameters were analyzed. RESULTS: The decannulated cases in group A and group B and group C were 22, 8, 13 respectively. The post-operative mean maximal glottic area was (47.2 +/- 7.4) mm2, (78.3 +/- 16.0) mm2, (48.1 +/- 6.5) mm2 respectively. Group B cases glottic area was larger than that of group A and group C (t value were 4.46 and 3.85, P value were 0.000 and 0.001). No significant difference was found between group A and group C (t = 1.68, P = 0.101). After surgery, in group A, 17 cases voice quality was the same compared with that of before surgery, and 7 cases voice quality had become worse; In group B, the voice quality had become better in 5 cases, completely recovered in 1 case, and had not change in 3 cases; In group C, the voice quality had become deteriorated in 10 cases and no change in 3 cases. And in group B, ipsilateral diaphragm paralysis in 9 cases after surgery, whose vital capacity and forced vital capacity had decreased to 72%-84%, 76%-84% of that before the surgery respectively; and the diaphragm mobility had recovered by 35%-76% respectively, while vital capacity and forced vital capacity had become 93%-97%, 91%-98% of that before the surgery. In Group B, all cases' pulmonary function was normal half a year postoperatively. CONCLUSIONS: Reinnervation of the posterior cricoarytenoid muscle by phrenic nerve seems to be best procedure with better post-operative voice and larger glottic area. Although the sufficient airway for decannulation can be acquired in Group A and Group C, but most of patients in Group A had pre-operative vocal level and badly abnormal in Group C.

[Intratumor bleomycin-A5 injection under electrolaryngoscope for treatment of large laryngopharyngeal and laryngeal hemangioma].

OBJECTIVE: To study the therapeutic effect of bleomycin-A5 injection under eletrolaryngoscope for treatment of large laryngopharyngeal and laryngeal hemangioma. METHODS: Intratumor bleomycin-A5 injection under eletrolaryngoscope was performed in 18 cases of large laryngopharyngeal and laryngeal hemangioma with surface anaesthesia, for totally 7 to 14 (mean 10.2) injections in each case. RESULTS: Twelve patients were cured and 6 showed obvious improvement. Follow-up of the patients for over one year found no recurrence of the hemangioma. CONCLUSION: Bleomycin-A5 injection is a minimal invasive procedure for treatment of large laryngopharyngeal and laryngeal hemangioma, causing less pain and better preserving the laryngeal function without the necessity of tracheotomy.

[Quality of life, personality, coping style in the patients with advanced laryngeal cancer].

OBJECTIVE: To evaluate the relationship between the life quality of advanced laryngeal squamous cell cancer patients and their personality, coping style and other psychological factors. METHODS: The life quality were measured for 2 sub-groups of advanced laryngeal cancer patients and the normal control group. The Eysenck personality questionnaire (EPQ), coping style questionnaires (CSQ) and University of Washington-quality of life (UW-QOL) were used for life quality evaluation. The 2 sub-groups of the patients on the worse speech, job and ability (group I), the better speech, job and ability (group II), and normal control. RESULTS: (1) UW-QOL score: the total, activity, recreation, job and speech scores of group II were significantly higher than those of group I (P < 0.01). Group II was better than group I in appearance (P < 0.05). (2) EPQ score: the P and N scores in group II were lower than that in group I (P < 0.05). The E scores in group II were significantly higher than that in group I (P < 0.01). (3) CSQ score: the problem-saving factor and help-seeking factor in group II were more significantly lower than that in group I (P < 0.01). The self-blaming factor in group II were higher than that in group I (P < 0.05). (4) There was positive correlation between total scores of QOL and the problem-saving factor, help-seeking factor of CSQ, the E scores of EPQ (P < 0.05), there was negative correlation between total scores of QOL and the P scores, the N scores of EPQ (P < 0.05). CONCLUSIONS: The advanced laryngeal cancer patients of group II have better life quality, and their personalities showed more extroversive, stable feeling, adaptable, mature coping styles. The above characteristics may have good effects on the prognosis of advanced laryngeal cancer.