Table 1 Sec proteins in human cancer

Sec61γ

Lu et al.⁸⁵

Glioblastoma

H80, HeLa

SEC61G is amplified and overexpressed in glioblastomas; SEC61G silencing suppresses cell growth and induces apoptosis; ER stress induces SEC61G expression

Sec62

Jung et al.⁸⁸

Prostate cancer

PC3, U145, DU145MN1

SEC62 copy-number gains in 50% of all prostate cancer samples+increased Sec62 protein level; however, copy-number gain in patients with lower risk of and longer time to progression

Greiner et al.⁸⁹

55 different tumor entities

DU145, PC3, LNCaP

SEC62 silencing sensitizes DU145, PC3 and LNCaP cells to thapsigargin treatment; correlation of thapsigargin sensitivity with SEC62 expression in DU145, PC3 and LNCaP cells; 72% of all tumors show SEC62 expression; SEC62 overexpression in tumor tissue compared with healthy tissue of the same organ in lung cancer (93–97%) and thyroid cancer (87–100%); SEC62 silencing reduces the migration of all tested cell lines

Greiner et al.⁹⁴

Prostate cancer

A549, H1299, HT1080, TX3868, PC3

SEC62 overexpression in the majority of prostate cancer cases correlating with the Gleason score

Linxweiler et al.⁹⁰

NSCLC thyroid cancer

A549, BC01, BHT101, ML1, HEK293

SEC62 overexpression in tumor tissue compared with healthy lung tissue; high expression levels correlate lymph node metastases and poor tumor differentiation; SEC62 silencing inhibits the migration of NSCLC cells; increased Sec62 protein (40%) and mRNA (60%) levels in thyroid cancer compared with tumor-free tissue; SEC62 silencing inhibits the migration of BC01, BHT101 and ML1 cells, and sensitizes the cells to thapsigargin-induced ER stress; SEC62 overexpression stimulates the migration of HEK293 cells

Weng et al.⁹³

HCC

/

High SEC62 expression in PBMCs correlates with reduced recurrent-free survival; Sec62 as an independent predictor of HCC recurrence

Linxweiler et al.⁶⁸

NSCLC

PC3, HeLa, A549, BC01, BHT101, ML1, HEK293

High SEC62 expression correlates with a poorer OS; effect of SEC62 silencing on tumor cell migration and ER stress tolerance can be mimicked by CaM anatgonists; SEC62 overexpression in HEK293 cells increases ER stress tolerance

Hagerstrand et al.¹⁰²

26 different tumor entities

T47D, HCC1937, H3255, HCC95, H1819, H26, TE6, RPMI8226, Fu-Ov-O1, COLO320, MCF7, MDA-MB-231, ZR75-1, HMEC, HCC364, DLD1, HMLE

3q26 amplification: 22% of tumor samples (43.7% in ovarian cancer, 31.7% in breast cancer, 31.2% in non-small-cell lung cancer). 3q26-encoded SEC62 is required for the proliferation of celll lines with 3q26 amplification; SEC62 overexpression in HMLE cells induces subcutaneous tumor growth in C.Cg/AnNTac-Foxn1^nunu mice; SEC62 expression level correlates wtih 3q26 amplification; SEC62 as a tumor-driver gene of the 3q26 region

Wemmert et al.⁹²

HNSCC

/

High Sec62 protein level is associated with poorer OS and PFS

Linxweiler et al.⁹¹

Cervical cancer

HeLa, MCF7

Stepwise increase in SEC62 expression depending on the severity of dysplasia with the highest expression in invasive cervical cancer; SEC62 silencing inhibits and SEC62 overexpression stimulates the migration of cervical cancer cells

Sec63

Mori et al.⁸²

Gastric cancer CRC

/

Frameshift mutations of the SEC63 gene due to microsatellite instability in 37.5% of gastric cancers and 48.8% of colorectal cancers

Schulmann et al.⁸³

HNPCC-associated SBC

/

Frameshift mutations of the SEC63 gene due to microsatellite instaibility in 56% of HNPCC-associated small-bowel cancers

Casper et al.⁸⁴

HCC

/

Microsatellite instability in the SEC63 gene in the tested HCC case; correlation of low hepatic SEC63 expression with decreased apoptosis and increased proliferation rate in the mouse model