TUBA1C

TUBA1C

A gene on chromosome 12q13.12 that encodes an alpha tubulin, which combines with a beta tubulin to form microtubules, acting as a scaffold to determine cell shape and providing a matrix for cell organelle and vesicle movement via motor proteins.
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A total of 24 CAD genes, namely, 105 (ADARB2), 183 (AGT), 1586 (CYP17A1), 1611 (DAP), 2917 (GRM7), 2982 (GUCY1A3), 4134 (MAP4), 4625 (MYH7), 4629 (MYH11), 5126 (PCSK2), 5522 (PPP2R2C), 9229 (DLGAP1), 9833 (MELK), 23544 (SEZ6L), 23551 (RASD2), 55017 (C14orf119), 55759 (WDR12), 56776 (FMN2), 60676 (PAPPA2), 60680 (CELF5), 84790 (TUBA1C), 127833 (SYT2), 133491 (C5orf47), and 259232 (NALCN), were identified in this coexpression network (Figure 2, Table S3).
In the pathogenesis of NAFLD&NASH in Figure 5, we identified eight genes having expression difference between normal liver cells and NAFLD&NASH, i.e., HIST2H2BE (p value [less than or equal to] 1.06 x [10.sup.-1]), RFC5 (p value [less than or equal to] 1.5 x [10.sup.-2]), HSPB1 (p value [less than or equal to] 6.6 x [10.sup.-2]), ZNF480 (p value [less than or equal to] 1.0 x [10.sup.-2]), TUBA1C (p value [less than or equal to] 3.48 x[ 10.sup.-]1), RPL30 (p value [less than or equal to] 1 x [10.sup.-3]), FRAT2 (p value [less than or equal to] 1.08 x [10.sup.-1]), and TRMT1 (p value [less than or equal to] 5.33 x [10.sup.-1]).
In the hepatocarcinogenesis of NAFLD&NASH in Figure 2, we also identified eight genes with differences in expression between NAFLD&NASH and HCC, i.e., HIST2H2BE (p value [less than or equal to] 1.00 x [10.sup.-3]), RFC5 (p value < 1.00 x [10.sup.-3]), HSPB1 (p value [less than or equal to] 1.00 x [10.sup.-3]), ZNF480 (p value [less than or equal to] 1.00 x [10.sup.-3]), TUBA1C (p value [less than or equal to] 1.00 x [10.sup.-3]), RPL30 (p value [less than or equal to] 1.00 x [10.sup.-3]), FRAT2 (p value [less than or equal to] 1.00 x [10.sup.-3]), and ALDOB (p value [less than or equal to] 1.5 x [10.sup.-2]).
Furthermore, androgen receptor (AR) directly inhibited apoptosis through the mediation of TUBA1C. Intriguingly, HSPB1 caused antiapoptosis without miR-214 silencing and RFC5 caused DNA repair function.
In addition, the dysregulation of TUBA1C caused by abnormal miR-122 silencing and the dysregulation of ALDOB caused by both hypermethylation and abnormal miR-21 silencing might facilitate tumor metastasis.
In addition, we also found nine genes that play a central role in the upper progression path of Figure 1(a), i.e., two DNA repair-related genes (histone cluster 2 (H2be; HIST2H2BE) and replication factor C5 (RFC5)), four apoptosis-related genes (heat shock 27-kDa protein 1 (HSPB1), zinc finger protein 480 (ZNF480), tubulin alpha 1c (TUBA1C), and ribosomal protein L30 (RPL30)), and three metabolism-related genes (aldolase B (ALDOB), frequently rearranged in advanced T-cell lymphomas 2 (FRAT2), and tRNA methyltransferase 1 (TRMT1)).
Interestingly, abnormal miR-21 can still be accumulated to induce the dysregulation of ALDOB, and abnormal miR-122 can also be accumulated to induce the dysregulation of TUBA1C, which might facilitate tumor metastasis and invasion in HCC, as shown in Figure 2.
Additionally, our results (Figure 3) show that the inhibited aging-related miRNA miR1-2 in stage 1 bladder cancer cells leads to miR1-2 dysregulation of genes including KPNA2, TUBA1C, HN1, PSMD11, PSMD12, and TK1, which influence cell proliferation, DNA repair, and metastasis.
The design of a multiple drug combination for treating stage 1 bladder cancer depends on a strategy of inhibiting the highly expressed genes ADRM1, COPS5, PSMD8, SUMO2, CALR, PDIA3, DNAJB11, HSPA5, RPN1, CUL1, HSP90B1, KPNA2, PSMD12, ECT2, TK1, TUBA1C, HN1, and ENO1; activating the suppressed genes UBC, JUN, RARRES3, and FOS; and suppressing the drug's effect on the nondifferentially expressed genes BAG6, HUWE1, PAAF1, PSMD10, FAF2, PCYT1A, and PSMD10.
The design of a multiple drug combination for treating stage 4 bladder cancer depends on a strategy of inhibiting the highly expressed genes ADRM1, COPS5, PSMD8, SUMO2, RNF126, CALR, PDIA3, DNAJB11, HSPA5, RPN1, HSP90AA1, HSPA1B, METTL23, RARRES3, KPNA2, PSMD12, ECT2, JUN, TK1, TUBA1C, HN1, and ENO1; activating the suppressed genes BCL3, FOS, UBC, and GTF2A1; and suppressing the drug's effect on the nondifferentially expressed genes, which are the same as those in stage 1 bladder cancer.
The bold proteins, including RARRES3, TUBA1C, PSMD8, HSPA1B, RPS20, CALR, PAAF1, and KPNA2, were the identified core network biomarkers.
The bold proteins RARRES3, TUBA1C, PSMD8, HSPA1B, RPS20, CALR, PAAF1, and KPNA2 were the identified core network biomarkers.